Rathore et al. reported a mechanism by which mitochondrial ROS activate PKCε (prevented by chelerythrine and PKCε deletion) with subsequent increase in NOX activity (prevented by apocynin and p47phox deletion) in the setting of hypoxia as a model of ischemia/reperfusion damage (e.g., as observed in myocardial infarction (MI) or stroke) [151]. The gene discussed is NCF1; the disease is myocardial infarction.