For example, a study of clinically ascertained patients with autosomal dominant familial hypercholesterolemia (FH) caused by pathogenic variants in the low-density lipoprotein receptor gene (LDLR) revealed that a LDL-C PGS (PGSLDL-C) constructed of common, genome-wide significant markers modified the low-density lipoprotein cholesterol (LDL-C) phenotype15,16. Here, LDLR is linked to familial hyperaldosteronism.