Most cases of FH are attributable to mutations in the LDLR gene (encoding the low-density lipoprotein receptor, LDLR) that account for more than 90% of cases, while a minor part has been linked to mutations in APOB, PCSK9, or in the LDLRAP1 genes (in homozygosis). Here, VLDLR is linked to familial hyperaldosteronism.