Conversely, our data showed that during hyperthermia treatment, ectopic expression of Cirbp completely or mostly rescued hyperthermia-induced reduction in the phosphorylation levels of ATM, Chk2, p53, ATR and Chk1, which thereby reversed hyperthermia-induced reduction in DNA damage repair ability of cancer cells and increase in cell apoptosis, ultimately leading to increased thermoresistance and tumor growth, indicating that Cirbp overexpression protects cancer cells against hyperthermia-induced DNA damage and cell death (Fig. 12). The gene discussed is ATM; the disease is neoplasm.