The candidate gene approach pinpoints several mutations responsible for FH and consequently CAD (Figure 1): A mutation in the LDL receptor (LDLR), a mutation in apolipoprotein B (ApoB), a gain of function mutation in proprotein convertase subtilisin/kexin type 9 (PCSK9) genes, and null mutations in the genes encoding LDLR adaptor protein 1 (LDLRAP1) and ATP-binding cassette sub-family G (ABCG) member 5 (ABCG5) or member 8 ABCG8 (Figure 1) [19]. The gene discussed is APOB; the disease is familial hyperaldosteronism.