Activated STAT3 enters the nucleus in the form of dimers and transcribes downstream target genes.[16] Research has shown that STAT3 activation can also occur through JAK‐independent mechanisms, such as phosphorylation of the Tyr705 site by pyruvate kinase M2.[17] In the past several years, studies have found that p‐STAT3 is associated with EGFR‐TKI resistance, and inhibition of the p‐STAT3 can enhance the sensitivity of lung cancer cells to EGFR‐TKIs.[18]. The gene discussed is EGFR; the disease is lung carcinoma.