However, many reported gene-drug, gene-diet, and gene-environment interactions have been shown to be potentially attributable wholly or in part to quantile-dependent expressivity for adiposity (56 examples of interactions [14]), postprandial lipemia (64 examples [23]), serum triglycerides (76 examples [15]), total cholesterol (22 examples [16]), high-density lipoprotein cholesterol (88 examples [17, 18]), adiponectin (15 examples [20]), leptin (16 examples [19]), plasminogen activator inhibitor type-1 (21 examples [21]), and C-reactive protein concentrations (50 examples [22]). Here, CRP is linked to hyperlipidemia.