Exploiting MET dysregulation in EGFR-addicted non-small-cell lung carcinoma: a further step toward personalized medicine

Patients affected by non-small-cell lung cancer (NSCLC) harboring epidermal growth factor receptor (EGFR) activating mutations derive a dramatic and essential clinical benefit from EGFR tyrosine kinase inhibitors (TKIs) therapy in terms of activity, efficacy and quality of life (1,2). Nevertheless, besides the important therapeutic impact of these targeted agents, EGFR-addicted diseases typically develop resistance under the selective pressure of TKIs, usually within 1 year of treatment.