Our data collectively suggests 1) Tβ4 overexpression enhances differentiation of mouse ES cells into functional cardiac myocytes in vitro and in vivo, 2) Tβ4-ESCs inhibit apoptosis through down-regulation of PTEN and upregulation of Akt in the infarcted myocardium, 3) transplantation of Tβ4-ESCs reduce fibrosis formation via inhibition of MMP-9 activation following MI, and 4) enhanced left ventricular function is obtained following transplantation of Tβ4-ESCs post-MI. Here, AKT1 is linked to myocardial infarction.