The mechanism may involve (1) direct deposition of Lp(a) on endothelial cells, promoting lipid uptake by macrophages and accelerating atherosclerosis; (2) induction of endothelial dysfunction by high levels of Lp(a); and (3) inhibition of fibrinolysis through competition with plasminogen while inhibiting tissue factor pathway inhibitor to promote thrombosis10. This evidence concerns the gene PLG and atherosclerosis.