The heterozygous form is characterized by the presence of one mutation in low-density lipoprotein receptor [LDLR] and apolipoprotein B [APOB] genes and gain-of-function mutations in the proprotein convertase subtilisin/kexin type 9 [PCSK9] gene), and the presence of two mutated alleles is responsible for a more severe homozygous FH (HoFH) phenotype. Here, LDLR is linked to familial hyperaldosteronism.