The results of in vitro and in vivo experiments indicated that the THN system‐induced double‐jump ROS production triggered extensive immunogenic cell death (ICD) in tumor cells and polarized M2 macrophages into M1 phenotype, relieving the immunosuppressive microenvironment after RT and activating the antitumor immune ability of CD8+ T cells. The gene discussed is CD8A; the disease is neoplasm.