LPA is highly homologous with plasminogen, can bind to the lysine sites available for plasminogen on the surface of fibrin, and thereby compete with plasminogen to interfere with the fibrinolytic process and inhibit its activation, which increases the formation of thrombosis, and finally promotes the atherogenesis and coronary artery disease pathogenesis [19, 20]. This evidence concerns the gene PLG and coronary artery disorder.