Less commonly, the FH phenotype may be caused by mutations in other genes, for example, in apolipoprotein B (apoB), (ligand for the LDLR), PCSK9 (encodes the enzyme proprotein convertase subtilisin/kexin type 9, involved in the regulation of the half-life of the LDL receptor), STAP1 or apoE [2]. Here, APOE is linked to familial hyperaldosteronism.