Heterozygous gene variations inherited in a Mendelian and an autosomal dominant fashion in apolipoprotein B (ApoB), LDL receptor (LDLR), and proprotein convertase subtilisin/kexin type 9 (PCSK9) account for nearly 70–95% of FH cases [4,5,6,7]. Here, PCSK9 is linked to familial hyperaldosteronism.