Our observation that accelerated turnover of cysteine oxidation in lung cancers is associated with the relative absence of DUOX1, and can in fact be attenuated by DUOX1 overexpression, suggests that DUOX1 plays an important role in prolonged cysteine oxidation in normal epithelial cells to mediate appropriate EGFR activation and recycling. This evidence concerns the gene DUOX1 and lung carcinoma.