Nuclear EGFR localization in response to EGF in DUOX1-deficient cancer cells was further verified by subcellular fractionation, showing that EGF stimulation increased the presence of EGFR (and its phosphorylated forms pEGFR-Y1068 and pEGFR-Y1101) in nuclear extracts of A549 cells, which was suppressed after DUOX1 overexpression (Fig. 2a). The gene discussed is EGFR; the disease is cancer.