In oncology, cGAS-STING activation contributes to antitumor effects by triggering spontaneous antitumor immunity, enhancing senescence in premalignant cells, facilitating conventional cancer therapy responses, and inducing RCD through IFN-dependent and IFN-independent pathways [15, 16, 82], establishing it as a tumor-suppressor pathway that can be therapeutically targeted. Here, STING1 is linked to neoplasm.