Genetic defects underlying FH affect key genes involved in LDL cholesterol metabolism and synthesis (Low Density Lipoprotein Receptor (LDL-R), Apolipoprotein B (apoB), Proprotein Convertase Subtilisin/Kexin type 9 (PCSK9) and low-density lipoprotein receptor adaptor protein 1 (LDLRAP1)) [6]. Here, APOB is linked to familial hyperaldosteronism.