When cells experience persistent DSBs or SSBs induced by chemotherapeutic agents, proteins such as ATM and p53 are activated, and these activated proteins directly phosphorylate CDC25 family members, inducing cell cycle arrest in tumor cells while influencing timely repair of DNA damage, ultimately reducing the therapeutic efficacy of chemotherapeutic agents on tumor cells and promoting cellular resistance [48]. The gene discussed is TP53; the disease is neoplasm.