The mechanism accounting for this effect likely relies on: (i) radiation-induced tumor inflammation and cell death, (ii) DC that phagocytize “released” cancer cell DNA capable of activating the Stimulator of IFN genes (STING) pathway, (iii) increased type 1 IFN-licensed DC that prime tumor-specific T cells and (iv) reactive T cells that home to and engage the tumor with strong effector function.72 This evidence concerns the gene STING1 and neoplasm.