Plasma levels of high-density lipoprotein (HDL) cholesterol are inversely related to the incidence of coronary heart disease and stroke. The lowering of low-density lipoprotein (LDL) cholesterol with statin therapy reduces the risk of atherosclerotic cardiovascular disease but only by about one third. These findings have led to the idea that raising HDL cholesterol might be a treatment for atherosclerosis. On the basis of the high-HDL phenotype of a human genetic deficiency of cholesteryl ester transfer protein (CETP),¹ a new class of drugs that inhibit CETP was developed.² Although the CETP inhibitor torcetrapib is effective at raising HDL cholesterol levels, it . . .