Mutation of ATM in humans leads to the condition ataxia telangiectasia (A-T), which is characterized by: progressive neurodegeneration; immunodeficiency; genomic instability; clinical radio-sensitivity; and a predisposition to cancer, in particular lymphomas as a result of inappropriate signaling following programmed DSBs during V(D)J recombination in T-cells [11,12]. The gene discussed is ATM; the disease is Ataxia-telangiectasia.