We observed an increase in Nrf2 and NOX4 expression in tracheal epithelial cells and infiltrated inflammatory cells, but an increased NOX4/Nrf2 redox imbalance, suggesting that the overexpression of the reactive oxygen species-generating enzyme NOX4 overcame the capacity to induce the Nrf2 as previously outlined in patients with lung fibrosis [46]. The gene discussed is NOX4; the disease is pulmonary fibrosis.