Foam cell formation, a critical early event in atherosclerosis [4], is a complex process involving chemokine-driven recruitment of monocytes and their differentiation to macrophages, production of ROS leading to the oxidation of LDL, uptake of such oxLDL by macrophages, and the efflux of cholesterol from foam cells to acceptors such as HDL or its key apolipoprotein ApoA1 and subsequent reverse cholesterol transport [4]. This evidence concerns the gene APOA1 and atherosclerosis.