The genetic pathogenesis of FH includes pathogenic variants in low-density lipoprotein receptor (LDLR), apolipoprotein B (APOB), and proprotein convertase subtilisin/kexin type 9 (PCSK9) genes, which result in impaired function of LDL receptor, defects in APOB causing impaired binding with the LDL receptor, and gain-of-function mutations in PCSK9 causing LDL receptor degradation, respectively. The gene discussed is APOB; the disease is familial hyperaldosteronism.