Development of resistance to TKIs erlotinib or gefitinib in NSCLC cells and patient tumors is often associated with abnormal expression and/or activation of oncogenic drivers MET, Alk, Vascular endothelial growth factor receptor (VEGFR), Fibroblast growth factor receptor (FGFR), Src and Abl TKs [23–25]. This evidence concerns the gene ALK and non-small cell lung carcinoma.