The initial discovery that noncoding genetic variants at a locus on chromosome 1p13.3 near SORT1 were highly significantly associated with LDL cholesterol (LDL-C; ref. 5) and coronary artery disease (CAD; ref. 6) was remarkable, because only previously known regulators of LDL-C metabolism, such as LDLR, APOB, and PCSK9, had comparably significant associations of common variants with LDL-C (7). The gene discussed is LDLR; the disease is coronary artery disorder.