In conclusion, our studies highlight the importance of disturbed redox-dependent mechanisms in controlling diverse EGFR functions in lung cancers in association with loss of DUOX1, and introduce the novel concept that enhanced turnover of EGFR cysteine oxidation in lung cancers, mediated by GSTP1-mediated S-glutathionylation and subsequent reduction, is responsible for enhanced nuclear EGFR localization and increased tumorigenic properties by kinase-independent functions. The gene discussed is EGFR; the disease is lung cancer.