Using bioassays to quantify DSBs visualized as foci of γH2AX, 53BP1, or pATM (phosphorylated ataxia telangiectasia mutated), Rube et al. (30) and Schuler et al. (31) reported a compromised repair of IR-induced DSBs in G0 lymphocytes of childhood cancer patients suffering from different tumor entities, most pronounced in patients developing life-threatening or even lethal normal-tissue toxicities. The gene discussed is ATM; the disease is neoplasm.