In rodent/rat and cellular models with myocardial ischemia/reperfusion (hypoxia/reoxygenation) injury, knockout of Kdm3a (coding for histone demethylase KDM3A) exacerbated myocardial injury and cardiac dysfunction, and deteriorated mitochondrial apoptosis and inflammation; conversely, overexpression of KDM3A could ameliorate such alterations by promoting ETS1 expression [106]. The gene discussed is KDM3A; the disease is myocardial ischemia.