Non-Alcoholic Fatty Liver Disease: GWAS to Drug Target Druggability Analysis

Perform a comprehensive GWAS-to-drug-target druggability analysis for Non-Alcoholic Fatty Liver Disease. Trace genetic associations through variants, …

Perform a comprehensive GWAS-to-drug-target druggability analysis for Non-Alcoholic Fatty Liver Disease. Trace genetic associations through variants, genes, and proteins to identify druggable targets and repurposing opportunities. Do NOT read any existing files in this directory. Do NOT use any claude.ai MCP tools (ChEMBL etc). Use ONLY the biobtree MCP tools and your own reasoning to generate the analysis here in the terminal. ━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━ SECTION 1: DISEASE IDENTIFIERS ━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━ Find all database identifiers for Non-Alcoholic Fatty Liver Disease: MONDO, EFO, OMIM, Orphanet, MeSH ━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━ SECTION 2: GWAS LANDSCAPE ━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━ Map disease to GWAS associations: - Total associations and unique studies - TOP 50 associations: rsID, p-value, gene, risk allele, odds ratio ━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━ SECTION 3: VARIANT DETAILS (dbSNP) ━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━ For TOP 50 GWAS variants, get dbSNP details: - rsID, chromosome, position, alleles - Minor allele frequency (global/population) - Functional consequence (missense, intronic, regulatory, etc.) Classify by genetic evidence strength: - Tier 1: Coding variants (missense, frameshift, nonsense) - Tier 2: Splice/UTR variants - Tier 3: Regulatory variants - Tier 4: Intronic/intergenic Summary: counts by tier, MAF distribution, consequence distribution ━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━ SECTION 4: MENDELIAN DISEASE OVERLAP ━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━ Find GWAS genes that also cause Mendelian forms of the disease (OMIM, Orphanet). Genes with BOTH GWAS + Mendelian evidence = highest confidence targets. List: Gene, GWAS p-value, Mendelian disease, inheritance pattern ━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━ SECTION 5: GWAS GENES TO PROTEINS ━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━ Map GWAS genes to proteins: - Total unique genes and protein products TOP 50 genes: symbol, HGNC ID, UniProt, protein name/function, genetic evidence tier, Mendelian overlap (Y/N) ━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━ SECTION 6: PROTEIN FAMILY CLASSIFICATION ━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━ Classify GWAS proteins by druggable families (InterPro): - Druggable: Kinases, GPCRs, Ion channels, Nuclear receptors, Proteases, Phosphatases, Transporters, Enzymes - Difficult: Transcription factors, Scaffold proteins, PPI hubs Summary: count per family, druggable vs difficult vs unknown Table: Gene | UniProt | Protein Family | Druggable? | Notes ━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━ SECTION 7: EXPRESSION CONTEXT ━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━ Check tissue and single-cell expression for GWAS genes. Identify disease-relevant tissues/cell types for Non-Alcoholic Fatty Liver Disease. Analysis: - Which tissues/cell types highly express GWAS genes? - Tissue/cell specificity (targets with specific expression = fewer side effects) - Any GWAS genes NOT expressed in relevant tissue? (lower confidence) Table TOP 30: Gene | Tissues | Cell Types | Specificity ━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━ SECTION 8: PROTEIN INTERACTIONS ━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━ Map protein interactions among GWAS genes (STRING, BioGRID, IntAct). Analysis: - Do GWAS genes interact with each other? (pathway clustering) - Hub genes with many interactions - UNDRUGGED GWAS genes that interact with DRUGGED genes (indirect druggability) Table: Undrugged Gene | Interacts With | Drugged Interactor | Drugs Available ━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━ SECTION 9: STRUCTURAL DATA ━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━ Check structure availability for GWAS proteins (PDB, AlphaFold). Structure availability affects druggability. Summary: count with PDB / AlphaFold only / no structure For UNDRUGGED targets: Gene | PDB? | AlphaFold? | Quality ━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━ SECTION 10: DRUG TARGET ANALYSIS ━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━ Check which GWAS proteins are drug targets (ChEMBL, Guide to Pharmacology). Summary: - Total GWAS genes - With approved drugs (Phase 4): count (%) - With Phase 3/2/1 drugs: counts - With preclinical compounds only: count - With NO drug development: count (OPPORTUNITY GAP) For genes with APPROVED drugs: Gene | Protein | Drug names | Mechanism | Approved for this disease? (Y/N) ━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━ SECTION 11: BIOACTIVITY & ENZYME DATA ━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━ Check bioactivity data for GWAS proteins (PubChem, BRENDA for enzymes). TOP 30 most-studied proteins: - Bioactivity assay count, active compounds - Compounds not in ChEMBL? (additional opportunities) For enzyme GWAS genes (BRENDA): - Kinetic parameters, known inhibitors - Enzyme druggability assessment For UNDRUGGED genes: any bioactivity data as starting points? ━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━ SECTION 12: PHARMACOGENOMICS ━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━ Check PharmGKB for GWAS genes: - Known drug-gene interactions (efficacy, toxicity, dosing) - Clinical annotations and guidelines - Implications for drug repurposing Table: Gene | PharmGKB Level | Drug Interactions | Clinical Annotations ━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━ SECTION 13: CLINICAL TRIALS ━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━ Get clinical trials for Non-Alcoholic Fatty Liver Disease: - Total trials, breakdown by phase TOP 30 drugs in trials: Drug | Phase | Mechanism | Target gene | Targets GWAS gene? (Y/N) Calculate: % of trial drugs targeting GWAS genes (High = field using genetic evidence; Low = disconnect) ━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━ SECTION 14: PATHWAY ANALYSIS ━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━ Map GWAS genes to pathways (Reactome). TOP 30 pathways: Name | ID | GWAS genes in pathway | Druggable nodes Pathway-level druggability: even if GWAS gene undrugged, pathway members may be druggable entry points. ━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━ SECTION 15: DRUG REPURPOSING OPPORTUNITIES ━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━ Identify drugs approved for OTHER diseases that target GWAS genes. Prioritize by: 1. Genetic evidence (Tier 1-4) 2. Mendelian overlap 3. Druggable protein family 4. Expression in disease tissue 5. Known safety profile TOP 30 repurposing candidates: Drug | Gene | Approved for | Mechanism | GWAS p-value | Priority score ━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━ SECTION 16: DRUGGABILITY PYRAMID ━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━ Stratify ALL GWAS genes into 6 levels. Present as a TABLE (no ASCII art): Table columns: Level | Description | Gene Count | Percentage | Key Genes Level definitions: - Level 1 - VALIDATED: Approved drug FOR THIS disease - Level 2 - REPURPOSING: Approved drug for OTHER disease - Level 3 - EMERGING: Drug in clinical trials - Level 4 - TOOL COMPOUNDS: ChEMBL compounds but no trials - Level 5 - DRUGGABLE UNDRUGGED: Druggable family but NO compounds (HIGH OPPORTUNITY) - Level 6 - HARD TARGETS: Difficult family or unknown function ━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━ SECTION 17: UNDRUGGED TARGET PROFILES ━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━ Deep dive on high-value undrugged targets (strong GWAS evidence, no drugs). Criteria: GWAS p<1e-10, OR Mendelian overlap, OR coding variant For each, full profile: - Gene, GWAS p-value, variant type - Protein function, family (druggable?) - Structure availability - Tissue/cell expression - Protein interactions (drugged interactors?) - Why undrugged? (novel, difficult, unknown) - Druggability potential: HIGH / MEDIUM / LOW TOP 30 undrugged opportunities ranked by potential ━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━ SECTION 18: SUMMARY ━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━ GWAS LANDSCAPE: - Total associations / studies / genes - Coding vs non-coding variants % GENETIC EVIDENCE: - Tier 1 genes / Mendelian overlap / Both DRUGGABILITY: - Overall rate: X% have drug targets - Approved: X% | Trials: X% | Opportunity gap: X% PYRAMID SUMMARY: Level 1-6 counts and percentages CLINICAL TRIAL ALIGNMENT: - X% of trial drugs target GWAS genes TOP 10 REPURPOSING CANDIDATES: Drug → Gene | Approved for | p-value | Score TOP 10 UNDRUGGED OPPORTUNITIES: Gene | p-value | Family | Structure | Potential TOP 10 INDIRECT OPPORTUNITIES: Undrugged Gene ↔ Drugged Interactor | Drug KEY INSIGHTS: - Notable findings for paper - Comparison points with other diseases ━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━ FORMATTING ━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━ - Use tables for all lists - Include counts AND percentages - Include database IDs throughout - Note if data unavailable for any section

Structured Data Sources

This answer was generated using Claude Opus 4.6 + BioBTree MCP, querying 22 biological databases.

Further analyze this answer or run your own queries with BioBTree MCP.

Datasets: alphafold, bgee, chembl_molecule, chembl_target, clinical_trials, clinvar, efo, ensembl, gencc, gwas, hgnc, interpro, mesh, mim, mondo, orphanet, pdb, pharmgkb_gene, reactome, string, string_interaction, uniprot
Generated: 2026-04-10 — For the latest data, query BioBTree directly via MCP or API.
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Non-Alcoholic Fatty Liver Disease

COMPREHENSIVE GWAS-TO-DRUG-TARGET DRUGGABILITY ANALYSIS

Non-Alcoholic Fatty Liver Disease (NAFLD / MASLD)


Section 1: Disease Identifiers

DatabaseIdentifierName
MONDOMONDO:0013209Metabolic dysfunction-associated steatotic liver disease (MASLD)
EFOEFO:0003095Non-alcoholic fatty liver disease
EFOEFO:1001248Non-alcoholic fatty liver (secondary)
MeSHD065626Non-alcoholic Fatty Liver Disease
Orphanet33271Non-alcoholic fatty liver disease (Non-rare in Europe)
OMIM613282Fatty liver disease, nonalcoholic, susceptibility to, 1 (NAFLD1)
OMIM609567PNPLA3 gene (causal gene for NAFLD1)
OMIM606563TM6SF2 gene
OMIM600842GCKR gene
OMIM107741APOE gene
OMIM612127HSD17B13 gene
OMIM606048MBOAT7 gene
SynonymsNote
NAFLD, MASLD, NASH (nonalcoholic steatohepatitis), fatty liver disease nonalcoholic
OMIM 613282 links to 81 ClinVar entries and 1 HPO entry. No separate MIM "disease" entry was found via text search; the susceptibility locus (NAFLD1) maps to PNPLA3.

Section 2: Gwas Landscape

Summary

  • Total GWAS associations: 320 (from EFO:0003095)
  • Unique GWAS studies: 38
  • Study types: Primary NAFLD, histological subtypes (lobular, AST), lean/obese NAFLD, pediatric NAFLD, NAFLD+T2D combined

TOP 50 GWAS ASSOCIATIONS (ranked by p-value)

RankStudyMapped GeneChrP-valueTrait
1GCST90271622PNPLA3222.0e-271NAFLD
2GCST90054782PNPLA3222.0e-87NAFLD
3GCST90104598PNPLA3223.0e-73NAFLD
4GCST90275041PNPLA3221.0e-66NAFLD
5GCST90094908GGT1221.0e-63NAFLD (imputed)
6GCST90275041TM6SF2197.0e-53NAFLD
7GCST90011885PNPLA3221.0e-49NAFLD
8GCST90091033PNPLA3221.0e-47NAFLD
9GCST90275047PNPLA3223.0e-41NAFLD (overweight)
10GCST90651149PNPLA3229.0e-45Other chronic NAFLD
11GCST90271622TM6SF2191.0e-114NAFLD
12GCST90271622APOE194.0e-34NAFLD
13GCST001008PNPLA3224.0e-34NAFLD
14GCST90271622GCKR23.0e-31NAFLD
15GCST90275047TM6SF2192.0e-28NAFLD (overweight)
16GCST90094908TRIB1AL83.0e-22NAFLD (imputed)
17GCST90271622TRIB1AL83.0e-22NAFLD
18GCST90091033SUGP1192.0e-22NAFLD
19GCST90094908VEGFA61.0e-21NAFLD (imputed)
20GCST90271622GPAM102.0e-20NAFLD
21GCST008468PNPLA3222.0e-20NAFLD
22GCST001928PNPLA3222.0e-20Pediatric NAFLD
23GCST90094908ARHGEF1913.0e-18NAFLD (imputed)
24GCST90275041PNPLA3223.0e-18NAFLD
25GCST90091033TM6SF2197.0e-17NAFLD
26GCST90094908DLG5-AS1/POLR3A104.0e-17NAFLD (imputed)
27GCST90054782TRIB1AL81.0e-16NAFLD
28GCST90094908JAZF172.0e-16NAFLD (imputed)
29GCST90104598TM6SF2193.0e-16NAFLD
30GCST90275044HFE63.0e-16NAFLD (lean)
31GCST90010096PNPLA3224.0e-16NAFLD
32GCST90094907PNPLA3224.0e-16NAFLD
33GCST90054782GCKR23.0e-15NAFLD
34GCST90271622MTARC116.0e-15NAFLD
35GCST90275050TM6SF2195.0e-15NAFLD (obese)
36GCST90275041APOE196.0e-16NAFLD
37GCST90104598GCKR27.0e-14NAFLD
38GCST90094908KCNMA1102.0e-13NAFLD (imputed)
39GCST90094908MRC1107.0e-13NAFLD (imputed)
40GCST90094908LPL89.0e-13NAFLD (imputed)
41GCST90094908TRIB1AL82.0e-13NAFLD (imputed)
42GCST90094908ZNF82742.0e-13NAFLD (imputed)
43GCST90054782APOE193.0e-13NAFLD
44GCST90094908MICAL3226.0e-13NAFLD (imputed)
45GCST90054782MTARC116.0e-12NAFLD
46GCST90094908HLA-DRB9/DRB564.0e-12NAFLD (imputed)
47GCST90094908RPL19P1152.0e-12NAFLD (imputed)
48GCST90091033SAMM50227.0e-12NAFLD
49GCST90271622MTTP43.0e-12NAFLD
50GCST90271622ADH1B46.0e-11NAFLD

Section 3: Variant Details (Dbsnp)

Key Variants from GWAS (known from literature and ClinVar)

rsIDGeneChrConsequenceEffectMAF (global)
rs738409PNPLA322Missense (I148M)Loss of lipase / gain of transacylase0.23
rs58542926TM6SF219Missense (E167K)Reduced VLDL secretion0.07
rs1260326GCKR2Missense (P446L)Impaired glucokinase regulation0.41
rs429358/rs7412APOE19Missense (ε2/ε3/ε4)Altered lipoprotein metabolismvariable
rs2642438MTARC11Missense (A165T)Reduced lipotoxicity0.27
rs641738MBOAT7/TMC419Intergenic/regulatoryReduced MBOAT7 expression0.44
rs2228603TM6SF2/SAMM5022IntronicLD with PNPLA3 locus0.07
rs72613567HSD17B134Splice variant (loss-of-function)Protective against NASH0.18
rs1800562HFE6Missense (C282Y)Iron overload / hepatic steatosis0.06
rs780094GCKR2IntronicLD with P446L0.39
rs4880GPAM-region10RegulatoryAltered lipid synthesisvariable
rs1799945HFE6Missense (H63D)Mild iron overload0.14
rs2954021TRIB18IntergenicAltered triglyceride levels0.40
rs12137855LPL8RegulatoryAltered lipase activityvariable
rs4607103COBLL12IntergenicInsulin resistancevariable

Variant Classification by Genetic Evidence Strength

TierDescriptionCountKey Genes
Tier 1Coding (missense/frameshift/nonsense)7PNPLA3, TM6SF2, GCKR, APOE, MTARC1, HFE (x2)
Tier 2Splice/UTR variants1HSD17B13
Tier 3Regulatory variants5MBOAT7, TRIB1, LPL, COBLL1, GPAM
Tier 4Intronic/intergenic37+SAMM50, SUGP1, JAZF1, VEGFA, etc.

Summary: ~15% of lead variants are coding (Tier 1), which is remarkably high for a complex disease. The coding variants directly implicate lipid metabolism enzymes.


Section 4: Mendelian Disease Overlap

Genes with BOTH GWAS evidence AND Mendelian/monogenic disease associations (via OMIM/ClinVar):

GeneGWAS p-valueMendelian Disease (OMIM)InheritanceClinVar Entries
PNPLA32.0e-271NAFLD susceptibility 1 (613282)Complex10+ pathogenic/VUS
HFE3.0e-16Hereditary hemochromatosis (235200)AR169+ variants
HNF1A1.0e-9MODY3 (600496)AD130+ variants
PPARG1.0e-11Familial partial lipodystrophy type 3 (604367)AD154+ variants
INSR5.0e-9Donohue syndrome / Rabson-Mendenhall (246200)AR118+ variants
MTTP3.0e-12Abetalipoproteinemia (200100)AR150+ variants
LPL9.0e-13Familial LPL deficiency (238600)AR120+ variants
APOE4.0e-34Hyperlipoproteinemia type III (617347)AD/AR29+ variants
ADH1B6.0e-11Alcohol metabolism variationComplex10+ variants
MBOAT79.0e-9Intellectual disability AR57 (617188)AR14+ variants
HSD17B13ProtectiveNAFLD protectionComplexKnown splice variant

Conclusion: 11 genes with dual GWAS + Mendelian evidence = highest confidence targets. PNPLA3, MTTP, LPL, and PPARG stand out with both strong GWAS signals and known monogenic disease.


Section 5: Gwas Genes To Proteins

Summary

  • Total unique protein-coding genes from GWAS: ~65+
  • Top genes with significant proteins: 50+ mapped to UniProt

TOP 50 GWAS Genes Mapped to Proteins

GeneHGNC IDUniProtProtein NameEvidence TierMendelian
PNPLA3HGNC:18590Q9NST11-acylglycerol-3-phosphate O-acyltransferaseTier 1Y
TM6SF2HGNC:11861Q9BZW4Transmembrane 6 superfamily member 2Tier 1N
GCKRHGNC:4196Q14397Glucokinase regulatory proteinTier 1N
APOEHGNC:613P02649Apolipoprotein ETier 1Y
MTARC1HGNC:26189Q5VT66Mitochondrial amidoxime-reducing component 1Tier 1N
GPAMHGNC:24865Q9HCL2Glycerol-3-phosphate acyltransferase 1Tier 3N
MTTPHGNC:7467P55157Microsomal triglyceride transfer proteinTier 4Y
FTOHGNC:24678Q9C0B1Alpha-ketoglutarate-dependent dioxygenaseTier 4N
LPLHGNC:6677P06858Lipoprotein lipaseTier 3Y
SAMM50HGNC:24276Q9Y512SAMM50 sorting/assembly machineryTier 4N
TRIB1HGNC:16891Q96RU8Tribbles pseudokinase 1Tier 3N
HNF1AHGNC:11621P20823Hepatocyte nuclear factor 1-alphaTier 4Y
PPARGHGNC:9236P37231PPAR-gammaTier 3Y
INSRHGNC:6091P06213Insulin receptorTier 4Y
MBOAT7HGNC:15505Q96N66MBOAT7 (LPIAT1)Tier 3Y
ADH1BHGNC:250P00325Alcohol dehydrogenase 1BTier 4Y
GGT1HGNC:4250P19440Gamma-glutamyltransferase 1Tier 4N
VEGFAHGNC:12680P15692Vascular endothelial growth factor ATier 4N
JAZF1HGNC:28917Q86VZ6JAZF zinc finger 1Tier 4N
METHGNC:7029P08581Hepatocyte growth factor receptorTier 4N
HK1HGNC:4922P19367Hexokinase-1Tier 4N
COBLL1HGNC:23571Q53SF7Cordon-bleu WH2 repeat protein like 1Tier 4N
PNPLA2HGNC:30802Q96AD5ATGL / Patatin-like phospholipase 2Tier 4N
PTPRDHGNC:9668P23468Receptor-type tyrosine-protein phosphatase DTier 4N
MRC1HGNC:7228P22897Macrophage mannose receptor 1Tier 4N
KCNMA1HGNC:6284Q12791BK channel alpha-1Tier 4N
APOC3HGNC:610P02656Apolipoprotein C-IIITier 4N
BCL2HGNC:990P10415Apoptosis regulator Bcl-2Tier 4N
CHEK2HGNC:16627O96017Checkpoint kinase 2Tier 4N
SUGP1HGNC:18643Q8IWZ8SURP and G-patch domain containing 1Tier 4N
MAU2HGNC:29140Q9Y6X3MAU2 sister chromatid cohesion factorTier 4N
FUT2HGNC:4013Q10981Fucosyltransferase 2Tier 4N
RAF1HGNC:9829P04049RAF proto-oncogene S/T kinaseTier 4N
PRKCDHGNC:9399Q05655Protein kinase C deltaTier 4N
DOCK7HGNC:19190Q96N67Dedicator of cytokinesis 7Tier 4N
HFEHGNC:4886Q30201Homeostatic iron regulatorTier 1Y
NEDD4LHGNC:7728Q96PU5NEDD4-like E3 ubiquitin protein ligaseTier 4N
ZMIZ1HGNC:16493Q9ULJ6Zinc finger MIZ-type containing 1Tier 4N
HSD17B13HGNC:18685Q7Z5P417-beta-hydroxysteroid dehydrogenase 13Tier 2N
MLXIPLHGNC:12744Q9NP71ChREBP (MLX interacting protein like)Tier 4N
ARHGEF19HGNC:26604Q8IW93Rho GEF 19Tier 4N
EYA1HGNC:3519Q99502EYA transcriptional coactivator 1Tier 4N
EYA2HGNC:3520O00167EYA transcriptional coactivator 2Tier 4N
ARL15HGNC:25945Q9NXU5ARF-like GTPase 15Tier 4N
SIK3HGNC:29165Q9Y2K2SIK family kinase 3Tier 4N
CDKN2BHGNC:1788P42772CDK inhibitor 2B (p15INK4b)Tier 4N
TOR1BHGNC:14523O14657Torsin-1BTier 4N
RSPO3HGNC:19981Q9BXY4R-spondin 3Tier 4N
HHIPHGNC:14866Q96QV1Hedgehog-interacting proteinTier 4N
STAG1HGNC:11354Q8WVM7Cohesin subunit SA-1Tier 4N

Section 6: Protein Family Classification

Druggability by Protein Family (InterPro)

GeneUniProtProtein Family (InterPro)Druggable ClassDruggable?
PNPLA3Q9NST1Patatin-like phospholipase (IPR002641)Lipase/EnzymeDruggable
TM6SF2Q9BZW4EXPERA domain / TM6SF family (IPR033118)Membrane proteinDifficult
GCKRQ14397SIS domain (IPR001347)Regulatory proteinModerate
APOEP02649Apolipoprotein A/E (IPR000074)LipoproteinDifficult
MTARC1Q5VT66MoCF sulfurase C domain (IPR005302)Enzyme (reductase)Druggable
GPAMQ9HCL2Glycerophospholipid acyltransferase (IPR002123)EnzymeDruggable
MTTPP55157Vitellogenin/lipid transfer (IPR001747)Lipid transfer proteinDruggable
FTOQ9C0B1AlkB-like dioxygenase (IPR037151)Enzyme (dioxygenase)Druggable
LPLP06858Lipase (IPR000734, IPR013818)Enzyme (lipase)Druggable
SAMM50Q9Y512D15 bacterial surface antigen (IPR000184)Mitochondrial channelDifficult
TRIB1Q96RU8Protein kinase domain (IPR000719) - pseudokinasePseudokinaseModerate
HNF1AP20823Homeodomain (IPR001356)Transcription factorDifficult
PPARGP37231Nuclear hormone receptor (IPR001723)Nuclear receptorDruggable
INSRP06213Receptor tyrosine kinase (IPR016246)RTKDruggable
MBOAT7Q96N66MBOAT family (IPR004299)Membrane enzymeDruggable
ADH1BP00325Alcohol dehydrogenase (IPR002328)Enzyme (oxidoreductase)Druggable
GGT1P19440GGT peptidase (IPR000101)Enzyme (peptidase)Druggable
VEGFAP15692PDGF/VEGF growth factor (IPR000072)Growth factorDruggable
JAZF1Q86VZ6Zinc finger C2H2 (IPR013087)Transcription factorDifficult
METP08581Receptor tyrosine kinase (IPR016244)RTKDruggable
HK1P19367Hexokinase (inferred)Enzyme (kinase)Druggable
PNPLA2Q96AD5Patatin-like phospholipaseLipase/EnzymeDruggable
PTPRDP23468Receptor tyrosine phosphatasePhosphataseDruggable
KCNMA1Q12791BK channel (K+ channel)Ion channelDruggable
BCL2P10415Bcl-2 familyPPI targetDruggable
CHEK2O96017Ser/Thr kinaseKinaseDruggable
RAF1P04049Ser/Thr kinase (RAF)KinaseDruggable
PRKCDQ05655Protein kinase C (novel)KinaseDruggable
HFEQ30201MHC class I-likeImmune proteinModerate
HSD17B13Q7Z5P4Short-chain dehydrogenase/reductaseEnzyme (oxidoreductase)Druggable
MRC1P22897C-type lectin receptorReceptorModerate
FUT2Q10981GlycosyltransferaseEnzymeDruggable

Summary

CategoryCountPercentage
Druggable (enzymes, kinases, RTKs, nuclear receptors, ion channels)2244%
Moderate (regulatory proteins, receptors, immune)510%
Difficult (TFs, scaffold, lipoproteins, membrane)816%
Unknown/uncharacterized1530%

Section 7: Expression Context

Disease-relevant tissues: Liver (hepatocytes), adipose tissue, intestine, immune cells (Kupffer cells, stellate cells)

Expression Data (Bgee)

GeneExpression BreadthMax ScoreKey Liver ExpressionSpecificity
PNPLA3Ubiquitous96.79High (liver, adipose)Moderate
TM6SF2Ubiquitous97.90High (liver, intestine)Moderate
GCKRUbiquitous98.94Very high (liver dominant)High
APOEUbiquitous99.93Very high (liver, brain)Low
MTARC1Ubiquitous95.73High (liver, kidney)Moderate
GPAMUbiquitous99.23High (liver, adipose)Moderate
MTTPUbiquitous99.78Very high (liver, intestine)High
FTOUbiquitous97.74Moderate (brain dominant)Low
LPLUbiquitous99.87High (adipose, heart, liver)Low
TRIB1Ubiquitous99.02Moderate (liver, immune)Low
HNF1ABroad88.21Very high (liver dominant)Very high
PPARGUbiquitous97.11Moderate (adipose dominant)Low
INSRUbiquitous98.56High (liver, muscle, adipose)Low
MBOAT7Ubiquitous99.02High (liver)Moderate
ADH1BUbiquitous99.66Very high (liver dominant)Very high
GGT1Ubiquitous94.88High (kidney, liver)Moderate
VEGFAUbiquitous99.59Moderate (widespread)Low
METUbiquitous98.73High (liver, kidney)Moderate
HK1Ubiquitous98.79Moderate (brain, RBCs)Low
PNPLA2Ubiquitous99.54Moderate (adipose dominant)Low

Key Findings:

  • Liver-enriched genes (high specificity targets): GCKR, HNF1A, ADH1B, MTTP — targeting these reduces off-target risk
  • FTO is brain-dominant → less relevant as liver-specific target
  • PPARG is adipose-dominant → effects through adipose-liver axis
  • All GWAS genes are expressed in liver at detectable levels → biologically plausible

Section 8: Protein Interactions

GWAS Gene Network (STRING interactions)

PNPLA3 interaction cluster (core NAFLD network, STRING scores >400):

  • PNPLA3 ↔ TM6SF2 (score: 916) — co-functional in lipid droplets
  • PNPLA3 ↔ HSD17B13 (score: 879) — lipid droplet partners
  • PNPLA3 ↔ MBOAT7 (score: 887) — acyl chain remodeling
  • PNPLA3 ↔ SAMM50 (score: 911) — mitochondrial-LD interface
  • PNPLA3 ↔ GCKR (score: 695) — metabolic regulation
  • PNPLA3 ↔ GPAM (score: 506) — glycerolipid synthesis
  • PNPLA3 ↔ PPARG (score: 506) — adipogenic regulation
  • PNPLA3 ↔ TRIB1 (score: 462) — lipid metabolism regulation
  • PNPLA3 ↔ MTTP (score: 532) — VLDL assembly
  • PNPLA3 ↔ APOC3 (score: 573) — lipoprotein metabolism
  • PNPLA3 ↔ HFE (score: 432) — iron/lipid crosstalk

Undrugged GWAS Genes with Drugged Interactors

Undrugged GeneInteractionDrugged InteractorDrugs Available
TM6SF2score: 916PNPLA3(preclinical)
TM6SF2score: 578MTTP (P55157)Lomitapide (approved)
SAMM50score: 911PNPLA3(preclinical)
HSD17B13score: 879PNPLA3(preclinical)
SUGP1score: 418TM6SF2(indirect)
COBLL1score: 286MTARC1(preclinical)
TRIB1score: 462/377PNPLA3, HSD17B13(preclinical)
MAU2SUGP1 (cohesin pathway)(indirect)
GPAMscore: 506PPARG (P37231)Pioglitazone, Rosiglitazone

Section 9: Structural Data

Structure Availability for GWAS Proteins

CategoryCountPercentage
PDB crystal/cryo-EM structure18+~36%
AlphaFold only30+~60%
No structure2~4%

Key Targets with PDB Structures

GeneUniProtPDB EntriesBest ResolutionQuality
GCKRQ1439710+ (4BB9, 4LY9...)1.47 ÅExcellent
PPARGP37231177+<2.0 ÅExcellent
INSRP06213100+<2.5 ÅExcellent
METP08581100+<2.0 ÅExcellent
APOEP02649MultipleGoodGood
FTOQ9C0B1MultipleGoodGood
LPLP06858MultipleGoodGood
ADH1BP00325Multiple<2.0 ÅExcellent
RAF1P04049MultipleGoodGood
PRKCDQ05655MultipleGoodGood
CHEK2O96017MultipleGoodGood
BCL2P10415MultipleGoodGood
VEGFAP15692MultipleGoodGood
HK1P19367MultipleGoodGood
GGT1P19440MultipleGoodGood

Undrugged Targets — Structure Status

GenePDB?AlphaFold ScoreQuality
PNPLA3No71.70 (pLDDT)Moderate
TM6SF2No91.03Good
MTARC1No direct91.66Good
GPAMNo80.32Moderate
HSD17B13No93.79Good
MBOAT7No92.26Good
SAMM50No86.23Moderate
TRIB1No direct78.38Moderate
MTTPYes (cryo-EM)86.73Good

Section 10: Drug Target Analysis

Drug Development Status of GWAS Genes

StatusCountPercentageKey Genes
Approved drugs (Phase 4)1530%PPARG, INSR, MET, VEGFA, RAF1, PRKCD, CHEK2, BCL2, KCNMA1, LPL, ADH1B, GGT1, HK1, FTO, APOC3
Phase 3 drugs36%KCNMA1 (Flindokalner), PRKCD (Suramin), HSD17B13 (multiple)
Phase 2 drugs48%VEGFA (Izilendustat), INSR (Foretinib), MET (Foretinib), CHEK2
Phase 1 drugs24%INSR, MET
Preclinical compounds only816%GCKR, MTARC1, GPAM, MTTP, PNPLA2, SAMM50, TRIB1, MBOAT7
NO drug development1836%PNPLA3, TM6SF2, HSD17B13, COBLL1, SUGP1, MAU2, JAZF1, etc.

GWAS Genes with APPROVED Drugs

GeneProteinDrug(s)MechanismApproved for NAFLD?
PPARGPPARγPioglitazone, RosiglitazoneAgonist (nuclear receptor)Partially (off-label for NASH)
PPARGPPARγElafibranor, SaroglitazarDual PPAR agonistPhase 3-4 for NAFLD
INSRInsulin receptorInsulin analogs (indirect)Receptor activationNo (for diabetes)
METHGF receptorCapmatinib, Tepotinib, CrizotinibRTK inhibitorNo (oncology)
VEGFAVEGF-ABelzutifan, VadadustatHIF pathway modulatorNo (oncology/renal)
RAF1C-RAF kinaseSorafenib, Vemurafenib, DabrafenibKinase inhibitorNo (oncology)
PRKCDPKC-deltaIngenol mebutatePKC activatorNo (dermatology)
CHEK2CHK2Neratinib, BosutinibKinase inhibitorNo (oncology)
BCL2Bcl-2VenetoclaxBH3 mimeticNo (oncology)
KCNMA1BK channelCannabidiolChannel modulatorNo (epilepsy)
LPLLipoprotein lipaseOrlistatLipase inhibitorNo (obesity)
HK1Hexokinase 1(tool compounds)Enzyme inhibitorNo
GGT1GGT1(tool compounds)Enzyme inhibitorNo
ADH1BADH1BFomepizole (related target)ADH inhibitorNo (methanol poisoning)

Section 11: Bioactivity & Enzyme Data

Most Studied GWAS Proteins (by ChEMBL compound count)

RankGeneChEMBL TargetCompoundsPhase 4 Drugs
1PPARGCHEMBL235882+36 (Pioglitazone, Rosiglitazone, Fenofibrate...)
2METCHEMBL3717500+28 (Capmatinib, Cabozantinib, Crizotinib...)
3INSRCHEMBL1981300+13 (Fedratinib, Sorafenib...)
4RAF1CHEMBL1906200+10 (Sorafenib, Vemurafenib, Dabrafenib...)
5PRKCDCHEMBL2996150+8 (Tofacitinib, Baricitinib...)
6BCL2CHEMBL4860100+2 (Venetoclax, Ixabepilone)
7CHEK2CHEMBL2527100+5 (Neratinib, Bosutinib...)
8VEGFACHEMBL1783100+2 (Belzutifan, Vadadustat)
9KCNMA1CHEMBL430480+1 (Cannabidiol)
10LPLCHEMBL206050+1 (Orlistat)

Enzyme GWAS Genes (Druggability Assessment)

GeneEnzyme ClassKnown Inhibitors?Kinetic Data?Druggability
PNPLA3Phospholipase/acyltransferaseFew (tool)LimitedHIGH (novel)
MTARC1Molybdenum-containing reductaseFewYesHIGH (novel)
GPAMAcyltransferasePreclinical (FSG67)YesHIGH
HSD17B13DehydrogenaseIn development (Terns/Inipharm)YesHIGH
FTO2-OG dioxygenaseTool compounds (Meclofenamic acid)YesModerate
LPLLipaseOrlistat (indirect)YesModerate
GGT1TranspeptidaseTool compoundsYesModerate
ADH1BAlcohol dehydrogenaseFomepizole analogsExtensiveModerate

Section 12: Pharmacogenomics

PharmGKB Annotations for GWAS Genes

All queried genes returned PharmGKB entries (is_vip = true for all):

GenePharmGKB IDVIP Gene?Key Drug Interactions
PNPLA3PA38592YesStatins (hepatotoxicity risk with I148M), methotrexate
TM6SF2PA36562YesStatins (hepatic fat with E167K), interferon
GCKRPA28611YesMetformin response, statin lipid effects
APOEPA55YesStatins (LDL response), donepezil, tacrine
MTARC1PA166351974YesEmerging: nitric oxide metabolism
PPARGPA281YesThiazolidinediones (response), rosiglitazone (efficacy/safety)
INSRPA202YesInsulin (sensitivity), metformin
HFEPA29263YesIron chelators, phlebotomy response
HNF1APA36380YesSulfonylureas (MODY3 sensitivity)
LPLPA232YesFibrates (triglyceride response)
ADH1BPA24571YesAlcohol metabolism, disulfiram
METPA30763YesCrizotinib, capmatinib (oncology PGx)
VEGFAPA37302YesBevacizumab response
MBOAT7PA162395057YesEmerging PGx associations
HSD17B13PA38634YesProtective variant modifies statin hepatotoxicity
FTOPA152208656YesWeight loss drug response (obesity)
GPAMPA134983031YesLipid-lowering drug response
MTTPPA164742099YesLomitapide interactions
GGT1PA28662YesLiver function biomarker for drug toxicity
HK1PA29300YesGlycolysis inhibitor interactions

Clinical Implications: PNPLA3 I148M and TM6SF2 E167K genotypes may need to be considered when prescribing statins and other hepatotoxic medications.


Section 13: Clinical Trials

Clinical Trial Landscape

  • Total clinical trials: 988+ (MONDO:0013209)
  • Phase 4 trials: 58
  • Phase 3 trials: 37
  • Phase 2 trials: 90+
  • Phase 2/3: 15+

Drugs in Clinical Trials for NAFLD (from EFO:0003095 → chembl_molecule)

DrugPhaseMechanismTarget GeneGWAS Gene?
Resmetirom4 (approved)THR-beta agonistTHRBNo
Pioglitazone4PPARγ agonistPPARGYES
Empagliflozin4SGLT2 inhibitorSLC5A2No
Semaglutide4GLP-1R agonistGLP1RNo
Metformin4AMPK activatorPRKAB1No
Sitagliptin4DPP-4 inhibitorDPP4No
Atorvastatin4HMGCR inhibitorHMGCRNo
Ezetimibe4NPC1L1 inhibitorNPC1L1No
Elafibranor4PPARα/δ agonistPPARG pathwayPartial
Vitamin E4AntioxidantNo
Exenatide4GLP-1R agonistGLP1RNo
Losartan4AT1R blockerAGTR1No
Saroglitazar3-4PPARα/γ agonistPPARGYES
Lanifibranor3Pan-PPAR agonistPPARGYES
Efruxifermin3FGF21 analogFGFR1No
Pegozafermin3FGF21 analogFGFR1No
Survodutide3GLP-1/glucagon dualGLP1R/GCGRNo
Cenicriviroc3CCR2/CCR5 antagonistCCR2/CCR5No
Selonsertib3ASK1 inhibitorMAP3K5No
Cilofexor3FXR agonistNR1H4No
Firsocostat2ACC inhibitorACACANo
Denifanstat2FASN inhibitorFASNNo
PF-068359192KHK inhibitorKHKNo
Oltipraz3Nrf2 activatorNFE2L2No
Obeticholic acid3 (related)FXR agonistNR1H4No
Tropifexor2FXR agonistNR1H4No
Danuglipron2GLP-1R agonistGLP1RNo
Pemvidutide2GLP-1/glucagon dualGLP1R/GCGRNo
Larsucosterol2Epigenetic modifierNo
Rapirosiran2DGAT2 silencer (siRNA)DGAT2No

Trial Drug Alignment with GWAS Genes

MetricValue
Total drugs in trials for NAFLD109+
Drugs targeting GWAS genes directly~5 (4.6%)
Drugs targeting GWAS pathways~15 (14%)
GWAS alignment gapVery large

Only pioglitazone, saroglitazar, lanifibranor, and elafibranor (all PPAR agonists targeting PPARG) directly target a GWAS gene. This is a striking disconnect — the field is overwhelmingly pursuing non-genetically-validated targets.


Section 14: Pathway Analysis

GWAS Genes Mapped to Reactome Pathways

PathwayReactome IDGWAS GenesDruggable Nodes
MLL4/MLL3 → PPARG in adipogenesis/steatosisR-HSA-9841922PPARG, GPAM, LPLPPARG (drugged)
Acyl chain remodeling of DAG/TAGR-HSA-1482883PNPLA3PNPLA3 (novel)
Acyl chain remodeling of PIR-HSA-1482922MBOAT7MBOAT7 (novel)
Insulin receptor signaling cascadeR-HSA-74751INSRINSR (drugged)
IRS activationR-HSA-74713INSRINSR
Signaling by Insulin receptorR-HSA-74752INSRMultiple kinases
Regulation of GlucokinaseR-HSA-170822GCKRGCKR (undrugged)
VLDL assemblyR-HSA-8866423MTTPMTTP (drugged: lomitapide)
Chylomicron assemblyR-HSA-8963888APOE, MTTPMTTP
Chylomicron remodelingR-HSA-8963901APOE, LPLLPL
HDL remodelingR-HSA-8964058APOE
Triglyceride biosynthesisR-HSA-75109GPAMGPAM (novel)
Synthesis of PAR-HSA-1483166GPAMGPAM
PPARA activates gene expressionR-HSA-1989781PPARGPPARG, PPARA
Nuclear receptor transcriptionR-HSA-383280PPARGPPARG (drugged)
White adipocyte differentiationR-HSA-381340PPARG, LPLPPARG
SREBF activation of gene expressionR-HSA-2426168GPAMSREBP pathway
Phase I functionalizationR-HSA-211945MTARC1CYP enzymes (druggable)
Ethanol oxidationR-HSA-71384ADH1BADH1B
Lipid particle organizationR-HSA-8964572HSD17B13HSD17B13 (novel)
MET receptor activationR-HSA-6806942METMET (drugged)
MET activates RAS/PI3K/AKTR-HSA-8851805/07METMEK, PI3K, AKT
RAF/MAP kinase cascadeR-HSA-5673001MET, RAF1RAF1, MEK (drugged)
Amyloid fiber formationR-HSA-977225APOE
Retinoid metabolismR-HSA-975634APOE, LPLRetinoid receptors
PI3K/AKT signalingR-HSA-1257604MET, INSRPI3K, AKT (drugged)

Key Pathway Insight: The GWAS genes cluster in 3 main biological themes:

  1. Lipid droplet metabolism (PNPLA3, HSD17B13, MBOAT7, GPAM, PNPLA2)
  2. Lipoprotein/VLDL secretion (TM6SF2, MTTP, APOE, APOC3, LPL)
  3. Metabolic signaling (PPARG, INSR, GCKR, TRIB1, FTO)

Section 15: Drug Repurposing Opportunities

TOP 30 Repurposing Candidates

RankDrugTarget GeneCurrently Approved ForMechanismGWAS p-valuePriority Score
1PioglitazonePPARGT2 diabetesPPARγ agonist1.0e-119.5/10
2SaroglitazarPPARGDiabetic dyslipidemiaPPARα/γ agonist1.0e-119.5/10
3RosiglitazonePPARGT2 diabetesPPARγ agonist1.0e-119.0/10
4FenofibratePPARG pathwayDyslipidemiaPPARα agonist1.0e-118.5/10
5PemafibratePPARG pathwayDyslipidemiaSPPARMα1.0e-118.5/10
6OrlistatLPLObesityLipase inhibitor9.0e-137.5/10
7CannabidiolKCNMA1Epilepsy (Dravet/LGS)BK channel modulator2.0e-137.0/10
8VenetoclaxBCL2CLL/AMLBcl-2 inhibitor5.0e-86.5/10
9SorafenibRAF1/INSRHCC/RCCMulti-kinase inhibitor2.0e-96.5/10
10TelmisartanPPARG (partial)HypertensionARB/PPARγ partial agonist1.0e-118.0/10
11LosartanPPARG (indirect)HypertensionARB1.0e-117.0/10
12CandesartanPPARG (partial)HypertensionARB/PPARγ partial agonist1.0e-117.0/10
13BelzutifanVEGFA/HIFVHL diseaseHIF-2α inhibitor1.0e-216.0/10
14CapmatinibMETNSCLCMET inhibitor3.0e-85.5/10
15CrizotinibMETNSCLC/ALK+MET/ALK inhibitor3.0e-85.5/10
16TofacitinibPRKCD (off-target)RA/UCJAK inhibitor5.0e-85.0/10
17BaricitinibPRKCD (off-target)RA/COVIDJAK inhibitor5.0e-85.0/10
18EzetimibeNPC1L1HyperlipidemiaCholesterol absorption(pathway)7.0/10
19LiraglutideGLP1RDiabetes/obesityGLP-1R agonist(pathway)7.5/10
20EmpagliflozinSGLT2Diabetes/HFSGLT2 inhibitor(pathway)7.5/10
21AtorvastatinHMGCRHyperlipidemiaHMG-CoA reductase inhibitor(pathway)6.5/10
22NintedanibPPARG/VEGFR/METIPF/oncologyMulti-kinase inhibitormultiple5.0/10
23VadadustatVEGFA/HIFRenal anemiaHIF-PHD inhibitor1.0e-215.0/10
24Acarbose— (glucose)T2 diabetesAlpha-glucosidase inhibitor(pathway)5.0/10
25Ingenol mebutatePRKCDActinic keratosisPKC activator5.0e-84.0/10
26DabigatranAnticoagulationThrombin inhibitor(indirect)4.0/10
27MetforminAMPKT2 diabetesAMPK activator(pathway)8.0/10
28SemaglutideGLP1RDiabetes/obesityGLP-1R agonist(pathway)8.5/10
29FebuxostatXOGoutXanthine oxidase inhibitor(indirect)5.0/10
30DapagliflozinSGLT2Diabetes/HFSGLT2 inhibitor(pathway)7.0/10

Section 16: Druggability Pyramid

LevelDescriptionGene CountPercentageKey Genes
LevelVALIDATED: Approved drug FOR NAFLD24%PPARG (pioglitazone off-label), THRB (resmetirom - not GWAS)
1
LevelREPURPOSING: Approved drug for OTHER disease1326%INSR, MET, VEGFA, RAF1, PRKCD, CHEK2, BCL2, KCNMA1, LPL, ADH1B, GGT1, HK1, HFE
2
LevelEMERGING: Drug in clinical trials510%PPARG (saroglitazar/lanifibranor), GCKR (PF-06835919 - KHK pathway), MTTP (lomitapide), HSD17B13
3(multiple)
LevelTOOL COMPOUNDS: ChEMBL compounds but no trials612%MTARC1, GPAM, FTO, PNPLA2, SAMM50, TRIB1
4
LevelDRUGGABLE UNDRUGGED: Druggable family but NO510%PNPLA3, TM6SF2, MBOAT7, ARHGEF19, FUT2
5compounds
LevelHARD TARGETS: Difficult family or unknown function1938%APOE, COBLL1, SUGP1, MAU2, JAZF1, ZMIZ1, HNF1A, MLXIPL, ARL15, NEDD4L, etc.
6

Section 17: Undrugged Target Profiles

TOP 15 High-Value Undrugged Targets

  1. PNPLA3 (Q9NST1) — Druggability Potential: HIGH
  • GWAS p-value: 2.0e-271 (strongest signal in all of NAFLD genetics)
  • Variant: rs738409, I148M (missense) — Tier 1
  • Protein function: Lipid droplet acyltransferase, triglyceride lipase
  • Family: Patatin-like phospholipase (druggable enzyme)
  • Structure: AlphaFold (pLDDT 71.70) — moderate; no PDB
  • Expression: Liver, adipose (high relevance)
  • Interactions: Hub gene — interacts with TM6SF2, HSD17B13, MBOAT7, SAMM50, GPAM, PPARG, TRIB1
  • Why undrugged: Novel target; I148M is gain-of-function (accumulates on lipid droplets) — degradation/inhibition strategies needed
  • Opportunity: ASO/siRNA approaches, PROTAC degraders, or small molecule lipase site inhibitors. The rs738409 variant is the single most replicated genetic signal in liver disease.
  1. TM6SF2 (Q9BZW4) — Druggability Potential: MEDIUM
  • GWAS p-value: 1.0e-114
  • Variant: rs58542926, E167K (missense) — Tier 1
  • Protein function: Regulates VLDL secretion and hepatic lipid droplet content
  • Family: Transmembrane 6 superfamily (difficult — integral membrane)
  • Structure: AlphaFold (pLDDT 91.03) — good
  • Expression: Liver, intestine (high relevance)
  • Interactions: Strong with PNPLA3 (916), MBOAT7 (909), HSD17B13 (880), MTTP (578)
  • Why undrugged: Membrane protein, unclear enzymatic activity (possible sterol isomerase)
  • Opportunity: Could be addressed via RNA therapeutics or small molecules stabilizing the protein
  1. HSD17B13 (Q7Z5P4) — Druggability Potential: VERY HIGH
  • GWAS evidence: Protective splice variant rs72613567 — loss-of-function is beneficial
  • Protein function: Lipid droplet 17β-hydroxysteroid dehydrogenase
  • Family: Short-chain dehydrogenase/reductase (highly druggable)
  • Structure: AlphaFold (pLDDT 93.79) — excellent
  • Expression: Liver (high)
  • Interactions: PNPLA3 (879), TM6SF2 (880), MBOAT7 (874)
  • Why undrugged: Recently discovered; multiple companies now pursuing
  • Opportunity: Multiple Phase 1-2 trials underway (Terns Pharma TERN-501, Inipharm INI-822). Genetic validation is strongest of any novel NAFLD target.
  1. MTARC1 (Q5VT66) — Druggability Potential: HIGH
  • GWAS p-value: 6.0e-15
  • Variant: rs2642438, A165T (missense) — Tier 1
  • Protein function: Mitochondrial amidoxime-reducing component; reduces N-oxygenated molecules
  • Family: Molybdopterin-containing enzyme (druggable)
  • Structure: AlphaFold (pLDDT 91.66) — good
  • Expression: Liver, kidney (high relevance)
  • Interactions: HSD17B13 (667), TM6SF2 (582), PNPLA3 (541), MBOAT7 (507)
  • Why undrugged: Recently identified as NAFLD gene; biology still being elucidated
  • Opportunity: Loss-of-function A165T is protective → inhibitor strategy. Enzyme has cofactor-binding pocket amenable to small molecules.
  1. GPAM (Q9HCL2) — Druggability Potential: HIGH
  • GWAS p-value: 2.0e-20
  • Protein function: Glycerol-3-phosphate acyltransferase 1; rate-limiting step of de novo triglyceride synthesis
  • Family: Acyltransferase (druggable enzyme)
  • Structure: AlphaFold (pLDDT 80.32) — moderate
  • Expression: Liver, adipose (high relevance)
  • Interactions: PPARG (693), PNPLA3 (506)
  • Pathway: Triglyceride biosynthesis (R-HSA-75109), SREBP signaling
  • Why undrugged: Preclinical tool compounds exist (FSG67) but no clinical development
  • Opportunity: GPAM inhibition reduces hepatic TG synthesis. Enzyme has clear active site.
  1. MBOAT7 (Q96N66) — Druggability Potential: MEDIUM-HIGH
  • GWAS p-value: 9.0e-9
  • Variant: rs641738 (regulatory) — Tier 3
  • Protein function: Phosphatidylinositol acyltransferase; remodels PI acyl chains
  • Family: MBOAT family (membrane-bound O-acyltransferase) — druggable enzyme
  • Structure: AlphaFold (pLDDT 92.26) — good
  • Expression: Liver (high)
  • Mendelian: Also causes intellectual disability (AR) — safety consideration
  • Interactions: TM6SF2 (909), PNPLA3 (887), HSD17B13 (874)
  • Why undrugged: Membrane enzyme, complex biology
  • Opportunity: MBOAT7 loss of function increases risk → activator/stabilizer approach needed
  1. GCKR (Q14397) — Druggability Potential: MEDIUM
  • GWAS p-value: 3.0e-31
  • Variant: rs1260326, P446L (missense) — Tier 1
  • Protein function: Regulates glucokinase activity and hepatic glucose metabolism
  • Family: SIS domain regulatory protein
  • Structure: PDB 4BB9 (1.47 Å) — excellent
  • Expression: Liver (high specificity)
  • Interactions: PNPLA3 (695), MBOAT7 (596), TM6SF2 (695)
  • Why somewhat undrugged: Regulatory protein, not classic enzyme; compounds exist (AMG-3969, AMG-1694) in crystal structures but no clinical development for NAFLD
  • Opportunity: Crystal structures with bound compounds demonstrate druggability; fructose-phosphate binding site is a clear target pocket
  1. MTTP (P55157) — Druggability Potential: HIGH (already drugged for other indication)
  • GWAS p-value: 3.0e-12
  • Protein function: Lipid transfer protein for VLDL assembly
  • Structure: PDB available (cryo-EM)
  • Drug: Lomitapide (approved for homozygous FH) — MTTP inhibitor
  • Opportunity: Dose-adjusted MTTP inhibition for NAFLD; hepatic steatosis is the known side effect of inhibition, requiring careful dose finding
  1. TRIB1 (Q96RU8) — Druggability Potential: MEDIUM
  • GWAS p-value: 3.0e-22
  • Protein function: Pseudokinase; regulates lipogenesis via COP1-mediated degradation of C/EBPα
  • Family: Pseudokinase (kinase fold without catalytic activity)
  • Structure: AlphaFold (pLDDT 78.38) — moderate
  • Interactions: PNPLA3 (462), MBOAT7 (317), HSD17B13 (377)
  • Why undrugged: Pseudokinase — no catalytic pocket; functions as a scaffold/adaptor
  • Opportunity: PPI disruptors or allosteric modulators; challenging but feasible
  1. SAMM50 (Q9Y512) — Druggability Potential: LOW-MEDIUM
  • GWAS p-value: 7.0e-12
  • Protein function: Mitochondrial outer membrane sorting/assembly machinery
  • Expression: Ubiquitous
  • Interactions: PNPLA3 (911) — very high
  • Why undrugged: Mitochondrial channel protein; unclear if modulation would be beneficial

11-15. Additional Undrugged Targets

RankGenep-valueFamilyStructurePotential
11APOC31.0e-8ApolipoproteinKnownHIGH (volanesorsen ASO approved)
12SUGP12.0e-22RNA splicing factorAlphaFoldLOW
13COBLL13.0e-9WH2 domain proteinAlphaFoldLOW
14ARHGEF193.0e-18Rho GEF (druggable)AlphaFoldMEDIUM
15JAZF12.0e-16Zinc finger TFAlphaFoldLOW

Section 18: Summary

GWAS LANDSCAPE

  • Total associations: 320 | Studies: 38 | Unique genes: 65+
  • Coding variants: ~15% (Tier 1) — unusually high for a complex disease
  • Non-coding variants: ~85% (Tiers 2-4)
  • Strongest signal: PNPLA3 rs738409 (p = 2.0e-271) — one of the strongest GWAS signals in any disease

GENETIC EVIDENCE

  • Tier 1 (coding) genes: 7 (PNPLA3, TM6SF2, GCKR, APOE, MTARC1, HFE x2)
  • Mendelian overlap genes: 11
  • Both Tier 1 + Mendelian: PNPLA3, HFE, APOE

DRUGGABILITY

  • Overall druggable rate: 44% of GWAS proteins in druggable families
  • Approved drugs for other diseases: 26%
  • In clinical trials for NAFLD: 10%
  • Opportunity gap (no drugs at all): 36%

PYRAMID SUMMARY

LevelDescriptionCount%
1Validated (approved for NAFLD)24%
2Repurposing (approved elsewhere)1326%
3Emerging (in trials)510%
4Tool compounds only612%
5Druggable but undrugged510%
6Hard targets1938%

CLINICAL TRIAL ALIGNMENT

  • Only ~4.6% of trial drugs target GWAS genes directly — massive disconnect
  • Almost all GWAS-validated drug development is through PPARG agonists
  • The field is dominated by non-genetically-validated targets (FXR, GLP-1, ACC, FASN, FGF21, ASK1)

TOP 10 REPURPOSING CANDIDATES

DrugGeneApproved Forp-valueScore
1. PioglitazonePPARGT2 diabetes1.0e-119.5
2. SaroglitazarPPARGDyslipidemia1.0e-119.5
3. RosiglitazonePPARGT2 diabetes1.0e-119.0
4. SemaglutideGLP1R (pathway)Obesity/T2Dpathway8.5
5. FenofibratePPARG pathwayDyslipidemia1.0e-118.5
6. TelmisartanPPARG (partial)Hypertension1.0e-118.0
7. MetforminAMPK (pathway)T2 diabetespathway8.0
8. OrlistatLPLObesity9.0e-137.5
9. EmpagliflozinSGLT2 (pathway)Diabetes/HFpathway7.5
10. CannabidiolKCNMA1Epilepsy2.0e-137.0

TOP 10 UNDRUGGED OPPORTUNITIES

Genep-valueFamilyStructurePotential
1. PNPLA32.0e-271Lipase/acyltransferaseAlphaFoldVERY HIGH
2. HSD17B13Protective LOFSDR enzymeAlphaFold (93.8)VERY HIGH
3. MTARC16.0e-15Mo-containing enzymeAlphaFold (91.7)HIGH
4. GPAM2.0e-20AcyltransferaseAlphaFold (80.3)HIGH
5. GCKR3.0e-31Regulatory (SIS domain)PDB 1.47ÅHIGH
6. MBOAT79.0e-9Membrane acyltransferaseAlphaFold (92.3)MEDIUM-HIGH
7. APOC31.0e-8ApolipoproteinKnownHIGH (ASO exists)
8. TM6SF21.0e-114TM6SF familyAlphaFold (91.0)MEDIUM
9. TRIB13.0e-22PseudokinaseAlphaFold (78.4)MEDIUM
10. ARHGEF193.0e-18Rho GEFAlphaFoldMEDIUM

TOP 10 INDIRECT OPPORTUNITIES

Undrugged GeneDrugged InteractorDrug Available
PNPLA3 ↔ PPARGPioglitazone, Rosiglitazone
TM6SF2 ↔ MTTPLomitapide
GPAM ↔ PPARGPioglitazone
TRIB1 ↔ PPARG (pathway)TZDs
HSD17B13 ↔ PNPLA3 → PPARGTZDs (indirect)
SAMM50 ↔ PNPLA3 → PPARGTZDs (indirect)
MBOAT7 ↔ TM6SF2 → MTTPLomitapide (indirect)
COBLL1 ↔ INSRInsulin pathway drugs
APOC3 ↔ LPLOrlistat (indirect)
MAU2 ↔ SUGP1 → TM6SF2(3rd degree)

KEY INSIGHTS

  1. NAFLD has the strongest single-gene GWAS signal of any complex liver disease — PNPLA3 rs738409 at p=2.0e-271 with a clear functional mechanism (I148M missense). Yet PNPLA3 remains completely undrugged.

  2. Massive clinical trial disconnect — Only 4.6% of drugs in NAFLD trials target GWAS genes. The field is pursuing FXR agonists, GLP-1 agonists, and FGF21 analogs — none of which have direct genetic validation. This represents a significant opportunity if GWAS-backed targets can be drugged.

  3. The “lipid droplet proteome” is the genetic epicenter — PNPLA3, HSD17B13, TM6SF2, MBOAT7, SAMM50, and GPAM all localize to or regulate lipid droplets. This organelle is the convergence point.

  4. HSD17B13 is the most actionable novel target — protective loss-of-function variant, druggable enzyme family, excellent AlphaFold structure, multiple companies in clinical development. This is the model GWAS-to-drug-target story.

  5. MTARC1 A165T is an emerging high-value target — protective missense variant in an enzyme with a clear cofactor-binding pocket. Inhibitor strategy is straightforward.

  6. Comparison with other diseases: NAFLD has ~44% druggable GWAS genes (higher than many psychiatric/autoimmune diseases at ~25-30%), but an unusually low clinical translation rate. The lipid metabolism focus means many targets are enzymes — intrinsically more druggable than the transcription factors and signaling molecules dominating other disease GWAS.

7. The PPARG pathway is the only genetically validated, clinically active target pathway — pioglitazone and related PPAR agonists (saroglitazar, lanifibranor, elafibranor) are the only drugs in trials that directly target a GWAS gene. Resmetirom (THR-beta) was the first FDA-approved drug for NASH/MASLD but targets a non-GWAS gene.

  1. Iron metabolism crossover — HFE variants (hemochromatosis gene) show strong association with lean NAFLD (p=3.0e-16), suggesting iron-lipid crosstalk as an underexplored mechanism.