Administration of FGF1, alone and more pronouncedly in combination with an inhibitor of mitogen-activated protein kinase (p38), has also been demonstrated to induce neonatal and adult rat cardiomyocyte proliferation in vitro (89) as well as in vivo after myocardial infarction in adult rats, resulting in reduced scar formation and improved cardiac function (90). The gene discussed is FGF1; the disease is myocardial infarction.