Background Since the discovery of epidermal growth factor receptor (EGFR) mutations in 2004 as a driver alteration in non-small-cell lung cancer (NSCLC), mono-therapy with EGFR tyrosine kinase inhibitors (TKIs) is the conventional therapy. Growing evidence demonstrates that single EGFR TKI hyper-activates signal transducer and activator of transcription 3 (STAT3) almost immediately after starting treatment. Methods We conducted clinical and preclinical studies of key components of signaling pathways limiting EGFR TKI
