To assess the hypothesis that lipid and eQTL associations are driven by the same variant, we assessed colocalization of each of the top eight GLGC HLC eGenes and the four relevant GLGC traits (Giambartolomei et al., 2014). Fifteen trait-eGene pairs exhibited moderate to strong evidence of colocalization (PP.H4.ABF) > 0.4; Table S8). In particular, VKORC1 showed strong evidence of colocalization in both HLCs (TG, PP.H4.ABF = 0.97; LDL-C, PP.H4.ABF = 0.52) and GTEx livers (TG, PP.H4.ABF = 0.98; LDL-C, PP.H4.ABF = 0.65) but not in iPSCs (TG, PP.H4.ABF = 0.07; LDL-C, PP.H4.ABF = 0.006). ANGPTL3 colocalized in HLCs with all four GLGC traits (LDL-C, PP.H4.ABF = 0.77; TG, PP.H4.ABF = 0.76; TC, PP.H4.ABF = 0.49; HDL-C, PP.H4.ABF = 0.48). ANGPTL3 did not show evidence of colocalization in iPSCs or GTEx livers (Table S8).
