The relationship between elevated plasma levels of LDLcholesterol (LDL-C) and the risk of atherosclerosis has been very well established ( 1-3 ). Clinical trials have shown that reduction of LDL-C constitutes a primary strategy for the prevention and regression of coronary heart disease ( 4 ). Plasma cholesterol levels are regulated by feedback mechanisms including exogenous cholesterol absorption through the gastrointestinal tract and endogenous cholesterol synthesis by various tissues. Several studies have shown that the amount of dietary cholesterol absorbed also infl uences endogenous cholesterol synthesis ( 5-7 ). The newly identifi ed Niemann-Pick C1-like 1 (NPC1L1) protein expressed at the apical membrane of enterocytes has been shown to play a crucial role in the absorption of cholesterol and plant sterol ( 8 ). Several physiological determinants and pharmacological agents modulate cholesterol homeostasis, including genetic factors, body weight, ezetimibe therapy, and 3-hydroxy-3-methylglutaryl CoA reductase (HMG-CoAR) inhibitors (statins) therapy, the rate-limiting step in the cholesterol biosynthesis pathway ( 9 ). For instance, obese subjects show an increase in cholesterol synthesis with an associated decrease in cholesterol absorption ( 10, 11 ). Ezetimibe therapy has been shown to reduce intestinal cholesterol absorption while reciprocally elevating synthesis ( 12 ). These fi ndings suggest the presence of a reciprocal relationship between cholesterol absorption and synthesis, as a change in one vector results in a compensatory and opposing change in the other. Although recent data suggest that statin therapy is associated