The autosomal dominant form of FH is mostly due to the heterozygous and homozygous states of pathogenic variants in the low-density lipoprotein receptor (LDLR), apolipoprotein B (APOB), and proprotein convertase subtilisin/kexin type 9 (PCSK9) genes. The gene discussed is APOB; the disease is familial hyperaldosteronism.