An endogenous induction of apo AI synthesis resulting in high plasma apo AI and HDL-C concentration has been identified as a cause of familial hyperalphalipoproteinemia which is characterized by a low death rate from CHD and prolonged life expectancy [8], while a low apo AI synthesis rate leads to hypoalphalipoproteinemia [9] that promotes atherogenesis. This evidence concerns the gene AOPEP and coronary artery disorder.