In order to maintain cholesterol homeostasis in the body, reverse cholesterol transport refers to a series of metabolic processes that transfer cholesterol from peripheral tissues to the liver. In this reverse transport, cholesterol is carried by high density lipoproteins (HDL), which is thought to account for the negative relationship between plasma HDL levels and atherosclerosis. In the prevention and treatment of vascular disease, an attempt to stimulate this transport process through the use of medicines appears to hold tremendous potential. There are currently very few medications that have the ability to alter the activity of the many elements involved in the process. Although the newer fibric acids are often unsuccessful as anion-exchange resins, clofibrate lowers cholesterol esterification. The physiological process of removing cholesterol from tissues may be improved by probucol, which directly enhances the mass and activity of cholesteryl ester transfer protein. The limited information now available on how medications affect reverse cholesterol transport should encourage researchers to find new treatments that target this antiatherogenic pathway.