First, EGFR-T790M mutation occurs during the treatment of EGFR-TKIs, which causes the loss of EGFR-TKIs activity and leads to drug resistance.[10,11] Second, the amplification of MET receptor tyrosine kinases leads to the activation of EGFR-independent downstream intracellular signaling, resulting in drug resistance.[12,13] In addition, there are still unclear mechanisms of resistance such as pathological type conversion (NSCLC to SCLC), KRAS, PIK3CA, TP53 and Rb1 mutations. This evidence concerns the gene MET and non-small cell lung carcinoma.