• Proliferation of cardiomyocytes, alleviation of apoptosis, restoration of the cardiac contraction rate, suppression of endoplasmic reticulum stress, excessive autophagy reaction, and reduction of myocardial infarct size mainly through low-molecular-weight FGF2 • Suppression of the maladaptive functions of TGFβ1. This evidence concerns the gene FGF2 and myocardial infarction.