In both rat and porcine model of MI, transplantation of Akt-engineered MSCs led to improved LVEF and reduced scar size and fibrosis; this is because not only were Akt-engineered MSCs more resistant to apoptosis [18, 91], Akt modification also enhanced MSC secretion of paracrine factors such as VEGF, IGF-1, and FGF-2 [92]. Here, AKT1 is linked to myocardial infarction.