Epidemiological evidence that elevated HDL cholesterol (HDL-C) is inversely associated with atherosclerotic cardiovascular disease (ASCVD) [7,8,9,10,11], combined with the discovery of mutations in the CETP gene that are associated with increased HDL-C and reduced LDL cholesterol (LDL-C) concentrations [12,13], launched interest in the development of agents to pharmacologically inhibit CETP. The gene discussed is CETP; the disease is atherosclerosis.