In contrast to NOX2, cardiomyocyte overexpression of NOX4 promotes M2 macrophage polarization, improving myocardial remodeling and survival in MI mice, while also increasing autophagy to cope with energy stress (Mongue-Din et al., 2017; Sciarretta et al., 2013). The gene discussed is NOX4; the disease is myocardial infarction.