The combination of DS with the STING agonist diABZI demonstrates enhanced anti-tumor efficacy via complementary mechanisms: (a) DS activates IFN-I signaling through a STING-independent pathway, while diABZI engages the canonical STING–IFN axis, generating dual signaling cascades that synergistically amplify IFN-I production; (b) DS inhibits lysosome-mediated STING degradation, thereby extending diABZI-driven STING activation; and (c) sustained IFN-I signaling enhances DCs-dependent T-cell priming while suppressing immunosuppressive cell populations, including Tregs and M-MDSCs. Here, IFNA1 is linked to neoplasm.