FH typically results from mutations in four alleles that primarily affect LDLR pathway function, including the low-density lipoprotein receptor, apolipoprotein B (APOB), proprotein convertase subtilisin/kexin type 9 (PCSK9) [6] and LDLR adapter protein 1 (LDLRAP1) genes [7, 8]. This evidence concerns the gene VLDLR and familial hyperaldosteronism.