However, tumor cells can evade cell death by modulating their DNA damage repair capacity, thereby altering their sensitivity to chemoradiotherapy.30 Previous studies have demonstrated that NPM1 SUMOylation regulates homologous recombination (HR) and non-homologous end joining (NHEJ) by recruiting DNA damage repair proteins such as RAD51, RAP80, and BRCA1, thus influencing tumor chemosensitivity.26 Specifically, upon DNA DSB, NPM1 SUMOylation facilitates the recruitment of RAD51 to the damage sites, a critical step in homologous recombination, which is essential for DSB repair. The gene discussed is RAD51; the disease is neoplasm.