Up to 80% of the FH patients have heterozygous loss-of-function (LoF) mutations in the LDLR (Berberich and Hegele, 2019); while a minority have LoF mutations in the receptor-binding functional segments of APOB (Andersen et al., 2016); or gain-of-function (GoF) mutations in PCSK9 (Abifadel et al., 2003). This evidence concerns the gene APOB and familial hyperaldosteronism.