For example, excessive ROS results in DNA damage and apoptosis in lung epithelial cells and drives IPF progression via triggering the activation and release of TGF-β1, which can accelerate ROS generation, existing inflammation, and lung scarring as well as suppress antioxidant gene expression by mediating the interaction of Smad3-ATF3 with Nrf2. Here, NFE2L2 is linked to idiopathic pulmonary fibrosis.