Moreover, siRNA-mediated knockdown of Nrf2 or inhibition of EGFR by AG1478 inhibited EGFR phosphorylation and Nrf2 protein expression, respectively, indicating that there was positive crosstalk between Nrf2 and EGFR under the tumor microenvironment-like conditions created by treatment with TGF-β and hypoxia/reoxygenation without direct EGF ligand stimulation or activation of the EGFR-Keap1 axis. The gene discussed is KEAP1; the disease is neoplasm.