This process enables DC maturation and activation, as well as cross-presentation of the tumor antigens, thus recruiting cytotoxic T cells to the TME.18,19 However, STING agonists alone induce pro-tumorigenic type-2 rather than anti-tumor type-1 immune responses, which limits their therapeutic potential20 and motivates the synergistic combination with TLR9 agonists to serve as a potent type-1 adjuvant, amplify innate and adaptive IFN-γ production, and significantly suppress tumor growth. This evidence concerns the gene STING1 and neoplasm.