Therefore, we investigated the influence of three important EGFR-TKI resistant mechanisms (HGF, c-MET amplification and EGFR-T790M) on PD-L1 expression and the immune escape capability of tumours before and after acquired EGFR-TKIs resistance, and explored the regulation mechanisms of PD-L1 in different resistant subtypes. This evidence concerns the gene CD274 and neoplasm.