Accumulating genetic data have shown that most FH cases result from a heterozygous pathogenic variant in three different genes which encode key proteins involved in the LDL receptor endocytic and recycling pathways, including the LDL receptor (LDLR), apolipoprotein B (APOB), and proprotein convertase subtilisin kexin 9 (PCSK9) [1,8]. This evidence concerns the gene APOB and familial hyperaldosteronism.