Whereas BMDMs with isolated deficiencies of ATM or DNA-PKcs exhibit a robust DDR, those with deficiencies in both ATM and DNA-PKcs (Scid:AtmC/C:Lyz2Cre/+) exhibit a near-complete abrogation of γ-H2AX and p-KAP-1 formation in response to infection with L. monocytogenes (Figure 1H). The gene discussed is PRKDC; the disease is infection.