Still, in our blood data, we also identified eQTSs for non-blood PGSs, including metabolite- and lipid-levels, anthropometric traits and diseases such as asthma, celiac disease and coronary artery disease (Supplementary Note; Supplementary Figure 13a–c; Supplementary Data 5). For example, 11 out of the 26 eQTS genes that were associated with the PGS for high-density lipoprotein levels (HDL41,42; all FDR<0.05; Figure 6c) have previously been linked to lipid or cholesterol metabolism (Supplementary Table 15). ABCA1 and ABCG1, which were positively correlated with the PGS for high HDL, mediate the efflux of cholesterol from macrophage foam cells and participate in HDL formation. In macrophages, downregulation of ABCA1 and ABCG1 reduces reverse cholesterol transport into the liver by HDL43 (Figure 6d). The PGS for high HDL was also negatively correlated with the expression of the low-density lipoprotein receptor LDLR (strongest eQTS P=3.35×10−20), mutations in which are known to cause familial hypercholesterolemia44. Similarly, SREBF2, the gene encoding the TF SREBP-2, which increases the expression of LDLR, was downregulated (strongest eQTS P=3.08×10−7). The negative correlation between SREBF2 expression and measured HDL levels has been described
