The overexpression of Nox4 in endothelial cells reduces hypertension, myocardial inflammation, and fibrosis in response to AngII [118,123], whereas the endothelial cell-specific loss of Nox4 exacerbates cardiac hypertrophy, dysfunction, and fibrosis in response to pressure overload [100]. The gene discussed is AGT; the disease is cardiac hypertrophy.