For example, at SORT1, an established locus associated with both LDL (low-density lipoprotein) cholesterol levels and coronary heart disease, a functional noncoding variant creates a novel CCAAT/enhancer binding protein (C/EBP) binding site, leading to changes in hepatic SORT1 expression and in turn, changes in circulating LDL cholesterol levels.2 Motivated by this and other examples, significant effort has been dedicated to identifying variants associated with changes in gene expression (expression quantitative trait loci; eQTLs) that are also associated with changes in plasma lipid levels. This evidence concerns the gene SORT1 and coronary artery disorder.