The main finding of this study were: (Mozaffarian et al., 2016) NPY was upregulated in both ischemic myocardium and H2O2-induced cardiomyocytes; (Chiong et al., 2011) NPY-KO reduced infarct size and improved cardiac function in MI rats; (Nabel and Braunwald, 2012) NPY deletion inhibited cardiomyocyte apoptosis in ischemic myocardium and hypoxia/H2O2-induced cardiomyocytes by NPY1R–miR-499–FoxO4 axis (Figure 11). The gene discussed is FOXO4; the disease is myocardial infarction.