We were particularly interested in the HLC eGenes, irrespective of whether they were found only in HLCs or were shared by iPSCs (i.e., not exclusive to HLCs), because of their potential to modulate hepatocyte lipid metabolism. We rank-ordered the identified GLGC HLC eGenes by strength of association, judged by eQTL P-value (Figure 2B). Among the top GLGC HLC eGenes, we deferred studying SYPL2 and IGF2R; for each of these genes, the best eQTL SNP is in weak LD with an extremely strongly lipid-associated SNP in the SORT1 locus (r2 = 0.01 between rs10857787 and rs12740374 in Europeans) and the LPA locus (r2 = 0.035 between rs3777404 and rs1564348 in Europeans), respectively—so strongly that the SYPL2 and IGF2R SNPs meet the statistical threshold of P < 5 × 10−8 for lipid association even though they are located in different loci than the SORT1 and LPA lead SNPs, simply by being in weak LD with them. We also deferred studying FUT2, since its best eQTL SNP is a coding variant in the gene. Among the other top GLGC HLC eGenes, we sought
