We proved that the acquired T790M EGFR mutation significantly rewired EGFR trafficking fates via switching EGFR interactors in response to TKI treatment, that is, TKI induced autophagy-mediated EGFR degradation in both TKI-resistant models but prompted EGFR recycling back to plasma membrane in NSCLC cells only possessing primary EGFR mutations (Fig. 6). This evidence concerns the gene EGFR and non-small cell lung carcinoma.