EMT is a process by which epithelial cells lose polarity and trans-differentiate into a mesenchymal phenotype; this process has been considered to reduce the clinical activity of gefitinib and erlotinib and the sensitivity of NSCLC cells to these drugs [25, 26].These results suggested that PD-L1-targeting immunotherapy in NSCLC patients with primary resistance to EGFR-TKIs might restore sensitivity to EGFR-TKIs by reversing the EMT phenotype. Here, EGFR is linked to non-small cell lung carcinoma.