A critical event in the development of atherosclerosis is the recruitment of macrophages to the underlying epithelial layer of blood vessel walls and the uncontrolled uptake of oxidized/modified cholesterol. Continued accumulation of oxidized/modified cholesterol by macrophages and an associated inflammatory response leads to foam cell formation and the initiation of atherosclerosis.1 Reversing the process of macrophage cholesterol accumulation and inhibiting inflammation in the blood vessel wall have been held out as potential novel treatments for atherosclerosis; however, other than injectable forms of apolipoprotein A1,2 no drugs that either enhance macrophage cholesterol efflux or inhibit inflammation have been validated in the clinic for the treatment of cardiovascular disease. The liver X receptors (LXRα and LXRβ), members of the nuclear hormone receptor superfamily of ligand-activated transcription factors, are promising drug targets for treating atherosclerosis because they regulate cholesterol efflux from macrophages at the transcriptional level …