Numerous phase I and II clinical trials in healthy volunteers [54] and patients with stable atherosclerotic CHD [50] or after an acute myocardial infraction [58] have demonstrated that CSL-112 enhances the levels of apoA-I and pre-β HDL, induces a marked increase in cholesterol efflux capacity and is well tolerated with no evidence of liver toxicity. The gene discussed is APOA1; the disease is coronary artery disorder.