Collectively, these findings suggest that altered EGFR internalization in DUOX1-deficient lung cancer cells is associated with enhanced GSTP1-mediated S-glutathionylation of EGFR-SOH and subsequent reduction to EGFR-SH, whereas such turnover of EGFR-SOH is delayed in DUOX1-expressing cells and is independent of GSTP1 (Fig. 4d). Here, DUOX1 is linked to lung cancer.