The effect of CSL112 to elevate concentrations of apoA-I and pre-β HDL results in a marked increase in CEC, as reported in phase I and validated in phase II clinical trials in healthy volunteers [81], patients with stable atherosclerotic coronary vascular disease [104], and after acute myocardial infarction [83.••••]. This evidence concerns the gene APOA1 and acute myocardial infarction.