The activation of NOX4 was along with the generation of hydrogen peroxide (H2O2), myofibroblast differentiation, contractility, and ECM production in response to TGF-β1 in human myofibroblasts, and therapeutic targeting NOX4 could protect animal models from injury-provoked pulmonary fibrosis [26]. This evidence concerns the gene TGFB1 and pulmonary fibrosis.