An imbalance between the levels of NOX4 and nuclear factor-erythroid 2-related factor 2 (NRF2) promotes the pathogenesis of lung fibrosis by enhancing cellular senescence in myofibroblasts, resulting in resistance to apoptosis and persistent fibrosis during IPF pathogenesis (80, 81). This evidence concerns the gene NFE2L2 and pulmonary fibrosis.