Since ATM plays such a key role in the DDR, the anti‐tumor effects of multiple ATM inhibitors (ATMis) have been widely investigated in both cancer cells and mouse models.[3] Recently, we reported that knockout of both the Fanconi Anemia (FA)/BRCA pathway and ATM strongly inhibits end resection and generates toxic levels of NHEJ, thereby resulting in cellular death by synthetic lethality (SL). The gene discussed is ATM; the disease is cancer.