Mutations in LDLR are detectable in 80%–85% of FH cases; when a molecular genetic cause of FH is known, mutations of APOB are found in 5%–7% of the patients; mutations in the PCSK9 gene are detectable in fewer than 5% of the cases, and mutations of LDLRAP1 occur in <1% of the cases [7,9,15,16,17]. Here, LDLR is linked to familial hyperaldosteronism.