BA strikingly reduced the IC50 of EGFR-TKIs against wt-EGFR by directly targeting EGFR to trigger EGFR-mediated autophagy-related cell death and cell cycle arrest, thus revealing a novel mechanism underlying the powerful antitumor effect of combined treatment in wt-EGFR NSCLC. This evidence concerns the gene EGFR and non-small cell lung carcinoma.