ATM and neoplasm: Importantly, knockdown of BUB1B/BUBR1 in the resistant T24R-ATM+/+ cells abrogated the tumor growth after the IR treatment, whereas T24R-ATM−/− cells did not grow, regardless of the BUB1B/BUBR1 knockdown after the IR treatment (Fig. 4n), consistently suggesting the crucial interaction between ATM and BUB1B/BUBR1 in the context of the resistance to DNA-damaging agents.