ATM and neoplasm: As shown in Fig. 6a–c, oxidized ATM promoted CSCs to initiate tumor formation and growth in nude mice; administering nude mice with KU60019 as well as UK5099 delayed tumorigenic ability and suppressed tumor growth; exogenous acetate had an antagonistic ability to KU60019 and UK5099 to fuel the initiation of tumor formation and tumor growth of tumor-burden mice treated in a dose-dependent manner (Fig. 6a–c).