This crosstalk has an important role in the pathogenesis of IPF as NOX4 promotes the generation of ROS, TGF-β-induced (myo)fibroblast activation and epithelial cell death, and the apoptotic resistant phenotype of senescence myofibroblasts in IPF [93,109,110]. The gene discussed is NOX4; the disease is idiopathic interstitial pneumonia.