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MET pathway dysregulation has been identified in several solid tumors including lung cancers. METderegulated NSCLC (non-small cell lung cancer) represents a molecularly defined lung cancer. METexon14 (METex14) mutations and high-level MET amplification represent primary, targetable oncogenic drivers. Type I MET tirosine kinase inhibitors (crizotinib, capmatinib, tepotinib, savolitinib, AMG-337) and type II (cabozantinib, glesatinib, merestinib) showed promising results in preclinical and clinical trials. The main challenge of targeted therapies is the development of acquired resistance. Resistance to MET tirosine kinase inhibitors (MET TKIs) depends on target mutations or upregulation of MET ligand expression. Several strategies are under investigation to overcome acquired resistance. *Correspondence to: Valentina Mazza, Department of Oncology-Hematology, AUSL Romagna, Rimini, Italy, E-mail: valemazza610@gmail.com

new-molecular-drivers-in-nsclc-the-role-of-met