FH is caused by mutations of different genes involved in LDL-C metabolism, such as those associated with loss of function of the gene coding for the LDL receptor (LDLR), or of the apolipoprotein B gene (APOB) or those associated with gain of function in the gene proprotein convertase subtilisin/kexin type 9 (PCSK9) [9,10,11]. This evidence concerns the gene APOB and familial hyperaldosteronism.