The epidermal growth factor receptor(EGFR)-tyrosine kinase inhibitor(TKI) constitselleckchem Ferrostatin-1utes a milestone for the system treatment of advanced EGFR-mutated non-small cell lung cancer(NSCLC) and make significant progrProstate cancer biomarkersess in postoperative adjuvant therapy of early EGFR-mutated non-small cell lung canceFUT-175生产商r(NSCLC)[1].Despite remarkable activity exerted by(EGFR)-tyrosine kinase inhibitor(TKI) in this clinical setting,several resistance mechanisms have been described[2,3].Among these,small cell lung cancer(SCLC) transformation has been recognized as one of mechanisms of resistance to EGFR-TKI in advanced lung adenocarcinoma with EGFR mutant,accounting for 5%～15%[4,5].since effective therapeutic strategies to apply in this circumstance are relatively lacking to date.Herein,we report the case of a patient who developed a SCLC switch as resistance mechanism to gefitinib for postoperative L858R-positive EGFR-mutated NSCLC after 4-year adjutant treatment.Moreover,we performed a literature review to summarize the underlying mechan…