Although the transgenic overexpression of Nox4 in cardiac myocytes was sufficient to promote macrophage recruitment to the heart and polarization towards the M2 phenotype that was associated with a modest reduction in cardiac hypertrophy, fibrosis, and mortality following myocardial infarction [101], endogenous Nox4 plays an indispensable role in cardiac inflammation and tissue damage in the infarcted heart, as mice with a global loss of Nox4 exhibited less myocardial infarction-induced macrophage infiltration, ischemic injury, cardiomyocyte hypertrophy, and oxidative stress [74]. This evidence concerns the gene NOX4 and myocardial infarction.