APOB and familial hyperaldosteronism: Genetic mutationsin the LDL receptor (LDLR) account for the majority of FH cases, whilemutations in apolipoprotein B (apoB) and proprotein convertasesubtilisin/kexin type 9 (PCSK9) account for a minority [3].Additionally, mutations in the LDLR adaptor protein-1 result in a rare form ofautosomal recessive FH (Fig. 1, Ref.