Strikingly, these observations were extended to cardiac contractile cells, where the inactivation of p16INK4a and ARF increased the capability of the whole heart in vivo and cardiomyocytes in vitro to regenerate or proliferate after ischemia, showing a functional recovery after injury, a smaller scars size and enhanced myocardial repair [21,22,81]. The gene discussed is CDKN2A; the disease is ischemia.