KIT and myocardial infarction: Zhang et al. (2012a) proved that c-kit + cardiac stem cell (CSC) preconditioning through HDAC inhibition with trichostatin could substantially increase c-kit + CSC-derived myocytes and microvessels and reinforce in vivo functional recovery of MI. However, it is still unclear if specific HDAC4 suppression can modulate CSCs to promote myocardial repair and maintain cardiac performance. HDAC inhibition facilitated c-kit + CSCs to be differentiated into cardiac lineage commitments in vitro, whereas HDAC4 overexpression weakened c-kit + CSC-derived cardiogenesis (Zhang et al., 2014).