In contrast, in response to chemotherapeutic drug-induced double-strand breaks, HITT is transcriptionally activated and translocated to the nucleus, where it binds ataxia telangiectasia-mutated and attenuates the DNA damage-repair process by inhibiting the recruitment and activation of ataxia telangiectasia-mutated at sites of DNA breakage (28). The gene discussed is PPP1R13B-DT; the disease is Ataxia-telangiectasia.