Mice with a knockout of Nrf2 (Nrf2−/−) show exaggerated pathological hypertrophy, fibrosis, and apoptosis, and accelerated transition to heart failure, whereas overexpression of Nrf2 suppresses ROS and protects cardiomyocytes and cardiac fibroblasts from stress-induced growth [155]. The gene discussed is NFE2L2; the disease is heart failure.