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So far, the mouse model showing reduction or delay of these diseases has not been described. We found that the disruption of <jats:italic>Aplf<\/jats:italic> in mice moderately attenuated DNA damage repair and, unexpectedly, impeded myeloid neoplasms after exposure to ionizing radiation (IR). Irradiated mutant mice showed higher rates of p53-dependent cell death, fewer chromosomal translocations, and a delay in malignancy-induced mortality. Simultaneous deficiency of p53 abrogated IR-induced apoptosis and the benefit of impaired DNA repair on mortality in irradiated <jats:italic>Aplf<\/jats:italic><jats:sup>\u2013\/\u2013<\/jats:sup> mice. Depletion of APLF in non-tumorigenic human cells also markedly reduced the risk of radiation-induced chromosomal aberrations. 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