Ionizing radiation activates the ATM (Ataxia-telangiectasia mutated) protein, a process that involves dimer dissociation, autophosphorylation, and phosphorylation of downstream proteins such as p53 and Chk2. High expression of ATM is associated with radiation resistance. Additionally, tumor cells exposed to radiation induce breaks in their own DNA by activating the expression of Caspase-activated DNase (CAD), leading to arrest in the G2 phase of the cell cycle and subsequent DNA damage repair. The gene discussed is TP53; the disease is neoplasm.