RT initiates dynamic changes that can augment the anti-tumor immune response by multiple mechanisms, including: (1) induction of immunogenic tumor cell death and release of tumor-specific antigens, (2) increased expression of immune susceptibility markers on surviving tumor cells (e.g., cGAS-STING activation of type I IFN response), (3) local release of inflammatory cytokines and damage-associated molecular patterns which increase immune cell trafficking and activation, and 4) temporary local depletion of RT-sensitive immune lineages including suppressor and effector lymphocytes [11–13]. This evidence concerns the gene CGAS and neoplasm.