In most of the genetically characterized cases, FH is caused by autosomal dominant loss-of-function mutations in the LDL receptor (LDLR) gene and, less frequently, by mutations in other genes, such as apolipoprotein (APO) B, proprotein convertase subtilisin/kexin type 9 (PCSK9), and APOE (2). This evidence concerns the gene LDLR and familial hyperaldosteronism.