Studies of rare Mendelian forms of CAD have shown how mutations in genes [low density lipoprotein receptor (LDLR), apolipoprotein B (ApoB), proprotein convertase subtilisin/kexin type 9 (PCSK9), low density lipoprotein receptor adaptor protein 1 (ARH), ATP-binding cassette, sub-family G (WHITE), member 5 (ABCG5), cytochrome P450, family 7, subfamily A, polypeptide 1 (CYP7A1)]10 involved in low-density lipoprotein and high-density lipoprotein metabolism/homeostasis can cause premature CAD, but these mutations are thought to explain a relatively minor fraction of familial CAD. This evidence concerns the gene PCSK9 and coronary artery disorder.