Another study demonstrated that a CCL2 competitor (PA508) reduced inflammatory monocyte recruitment, limited neointimal hyperplasia, and attenuated myocardial ischemia/reperfusion injury in an Apolipoprotein E knock-out (Apoe−/−) mouse model, highlighting the potential of PA508 as novel therapeutic approach to treat MI (13). This evidence concerns the gene APOE and myocardial ischemia.