Alterations in the EGFR itself, somatic mutation or ALK rearrangement, and activation of alternative signalling pathways have been shown to induce acquired TKI resistance in EGFR‐mutant NSCLC.42 In several studies, EGFR inhibition with TKI concurrently activated STAT3 signalling in EGFR‐mutant lung cancer cells,28, 38, 43 by which cancer cells could utilize an alternative signalling pathway to evade the drugs designed for ‘addition oncogene’ EGFR. This evidence concerns the gene STAT3 and lung carcinoma.