Monocyte-derived macrophages are among the first cells to accumulate in atherosclerotic lesions. Primarily, they appear to scavenge lipids and lipoproteins from fatty streaks, but their long-term presence and accumulation of cholesterol and cholesteryl esters is the hallmark of atherosclerosis. Atherogenesis begins by a perturbation in the endothelium. Subsequently, blood monocytes and later T lymphocytes adhere to the endothelium and migrate into the intima. Macrophages accumulate cholesteryl esters and triglyceride in cytoplasmic droplets, leading to the formation of foam cells. Although questions still remain regarding the relative contribution of environmental and/or genetic factors to the cholesterol accumulation and initiation of the atherosclerotic process, it is believed that foam cell development and ultimately atherosclerosis result from a defective control in the intimal round-trip of cholesterol.