Molecular bases of FH are related to an impaired LDL uptake by the LDL receptor (LDLR), a condition genetically inherited mainly through pathogenic variants in the genes encoding for LDLR (LDLR gene), apolipoprotein B (ApoB—APOB gene) and Proprotein Convertase Subtilisin/Kexin Type 9 (PCSK9 gene) [1]. Here, LDLR is linked to familial hyperaldosteronism.