Nox‐4‐derived reactive oxygen species act as an intracellular signaling molecule downstream of TGF‐β receptor ligation, responsible for activation of redox‐sensitive tyrosine kinases and transcription factors including HIF‐1α Inhibition of Nox‐4 activity attenuates TGF‐β induced responses associated with pulmonary fibrosis and vascular remodeling (Jarman et al. 2014). This evidence concerns the gene NOX4 and pulmonary fibrosis.