FH is most often due to carriage of a mutation in the LDLR gene, which encodes the low-density lipoprotein receptor (LDL-R), but mutations in apolipoprotein B (APOB), and proprotein convertase subtilisin/kexin type 9 (PCSK9), can produce a phenotype identical to FH due to mutation in LDLR [6]. This evidence concerns the gene LDLR and familial hyperaldosteronism.