However, the NSCLC with mutant EGFR is not necessarily more sensitive to radiation (94), since the mutant EGFR can trigger the downstream pathways, including extracellular signal-regulated kinase (RAS/ERK), p38MAPK, c-Jun N-terminal kinase (JNK), and ERK5, and also activate PI3K/AKT/mTOR signaling pathway, leading to cell proliferation and anti-apoptosis, migration, DNA repair, cell cycle arrest, etc., which in turn increases the radioresistance of NSCLC (22, 23, 103, 105–108). This evidence concerns the gene MTOR and non-small cell lung carcinoma.