Autosomal dominant familial hypercholesterolemia (FH), defined by elevated LDL (low density lipoprotein) levels in which 70–95% of cases result from mutations in one of three genes (apolipoprotein B [APOB], low-density lipoprotein receptor [LDLR], proprotein convertase subtilisin/kexin type 9 [PCSK9]) [2], is associated with a substantial increase in coronary heart disease and atherosclerotic cardiovascular disease [3] and affects roughly 1 in 250 U.S. adults [4]. Here, LDLR is linked to familial hyperaldosteronism.