Radiotherapy instigates cell death by causing ionizing radiation-induced double-strand breaks (DSBs) in the DNA, which initiates the DNA damage response (DDR) leading to cell cycle arrest and repair of the damage or, if repair is unsuccessful, cell death. Two early, integral components in this pathway are ataxia telangiectasia mutated (ATM), a serine/threonine protein kinase belonging to the phosphatidylinositol 3-kinase-like (PIKK) family  and the MRN complex, a trimer of MRE11 (meiotic recombination 11), RAD50 and NBS1 molecules. The latter complex binds to the DSBs and generates regions of single stranded DNA with its nuclease activity, which then recruits ATM to the site of genetic damage. ATM in turn affects cell cycle arrest .