To explore whether the progression to NASH and fibrosis associated with the deletion of Nox4 might be ascribed to decreased NOX4-derived ROS generation and antioxidant defense, we examined whether the NOX1/4 inhibitor GKT137831 could promote NASH and fibrosis in HFD-fed C57BL/6 mice (Figure 13). The gene discussed is NOX1; the disease is metabolic dysfunction-associated steatohepatitis.