Feedback activation of STAT3 plays a prominent role in mediating drug resistance to a broad spectrum of targeted cancer therapies and chemotherapies.46 This feedback activation not only has been found in EGFR‐mutant NSCLC, but also in NSCLC patients with wide‐type EGFR,47 which may partly contribute to the intrinsic resistance and high recurrence with TKI treatment. The gene discussed is STAT3; the disease is non-small cell lung carcinoma.