Since Muller described, back in 1938, xanthomas collections, raised serum cholesterol and myocardial infarction (MI) [1] and later in the 1970s Brown and Goldstein reported the defects in the low-density lipoprotein receptor (LDLR) as the etiology of familial hypercholesterolemia (FH) [2], our understanding of FH has grown tremendously. This evidence concerns the gene VLDLR and familial hyperaldosteronism.