As we well known, FH has been classified into heterozygous and homozygous forms depending on the presence of affected alleles in genes encoding the LDL receptor (LDLR), apolipoprotein B (ApoB), and proprotein convertase subtilisin/kexin type 9 (PCSK9) [1, 2]. This evidence concerns the gene APOB and familial hyperaldosteronism.