We used coloc v2.3-1 29 to test for colocalisation between molecular QTLs and GWAS hits from Alzheimer’s disease 79, celiac disease 80, inflammatory bowel disease, ulcerative colitis, and Crohn’s disease 81, multiple sclerosis 82, 83, narcolepsy 83, primary biliary cirrhosis 84, psoriasis 85, rheumatoid arthritis 86, schizophrenia 87, systemic lupus erythematosus 88, type 1 diabetes 89 and type 2 diabetes 90. We ran coloc on a 250 Kb region centered on the eQTL gene for all eQTL variants that were less than 100 Kb away from at least one GWAS variant with nominal P < 1x 10-5. We then applied a set of filtering steps to identify a stringent set of eQTLs that colocalised with GWAS hits. We removed all cases with <50 SNPs in the cis region and selected only loci where PP3 + PP4> 0.5 and PP4/(PP3+PP4) > 0.5 to only keep loci where coloc strongly preferred a model of QTL for both traits, of a single shared causal variant driving both association signals over a model of two distinct causal variants. We excluded all colocalisation results from
