It has long been known that a low level of HDL cholesterol is a powerful independent predictor of increased cardiovascular risk, even among patients with LDL cholesterol levels below 70 mg/dl. In fact, a 1 mg/dl (0.026 mM) increment in HDL-C levels was associated with a significant decrease in the risk of coronary heart disease (CAD) of 2% in men and 3% in women. HDL-C has been proposed to have several anti-atherosclerotic properties, including the ability to mediate reverse cholesterol transport (RCT), antioxidant capacity, anti-inflammatory properties, nitric oxide-promoting activity, and an ability to transport proteins with their own intrinsic biological activities. RCT describes the metabolism and an important antiatherogenic function of HDL, namely, the HDL-mediated efflux of cholesterol from cells of the arterial wall and its subsequent delivery to the liver and steroidogenic organs, thus preventing atherosclerosis. HDL particles are responsible for RCT, as critical acceptors of cholesterol from lipid-laden macrophages and thereby play an important role in the maintenance of net cholesterol balance in the arterial wall and in the reduction of pro-inflammatory responses by lipid-rich macrophages. The antiatherogenic properties of HDL have been primarily ascribed to RCT. Khera et al. recently reported that HDL efflux capacity was inversely and significantly correlated with carotid intima-media thickness (CIMT). A one-standard deviation increase in HDL efflux capacity predicted a 30% reduction in the odds for CAD. Although cholesterol efflux from macrophages represents only a small portion of total RCT, the cholesterol efflux from macrophage foam cells is probably the most relevant step with respect to preventing or reversing atherosclerosis. HDL can be separated into two major parts, i.e., pre β-(further distinguished into preβ1-, preβ2-,preβ3-HDL) and a-HDL(separated into 5 distinct subclasses HDL3c 3b 3a 2a 2b). It has been postulated that RCT indeed was the metabolic process that nascent preβ-HDL converted to mature a-HDL, following the route of preβ1-HDL→preβ2-HDL→preβ3-HDL→HDL3→HDL2[13].