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 EGFR and head and neck squamous cell carcinoma.