Genetic mutations in FH patients have been detected in LDLR, APOB, and PCSK9, and are either in a heterozygous (HeFH) or homozygous (HoFH) FH form (Chiou and Charng, 2016; Sturm et al., 2018, Di Taranto et al., 2020; Nawawi et al., 2020). This evidence concerns the gene APOB and familial hyperaldosteronism.