Two observations paved the way to further investigate the radioresistance mechanism linked to RTKs: (1) RTKs, particularly, c-Met and EGFR, have been associated with radiation resistance in several malignancies such as HNSCC, NSCLC, and GBM (52, 53); (2) preclinical data indicated that radioresistance due RTK activation was mediated by DNA repair protein activation or by apoptosis inhibition (24, 27). This evidence concerns the gene MET and glioblastoma.