These results suggest that inhibition of HDAC can maintain cardiac function and attenuate cardiac remodeling by stimulating endogenous cardiac regeneration.241–246 In the context of ischemia/reperfusion injury and myocardial infarction, HDAC inhibitors valproic acid, tributyl butyrate, and suberoylanilide hydroxamic acid (SAHA) reduce myocardial infarction size and ventricular remodeling by inhibiting HDAC, and induce increased angiogenic response.47,247,248 Studies have demonstrated that long-term use of low doses of SAHA ameliorated cardiac remodeling after infarction. The gene discussed is HDAC9; the disease is myocardial infarction.