ATM as a key modulator in the networks of cell cycle checkpoints and DDR initiates a series phosphorylation cascades including CHK1/2, BRAC1/2, MDC1, γ‐H2AX and 53BP174, 133 ATM deletion is proved to enhance tumor radiosensitivity in p53‐deficient DIPG,134 and its inhibitor AZD1390 is currently involved in a clinical trial of the brain cancer patients underwent radiation therapy (NCT03423628). The gene discussed is ATM; the disease is neoplasm.