In conclusion, the killing effect of RC48 on colon cancer cells was triggered by its two components: On the one hand, MMAE, a tubulin inhibitor, arrested the cell cycle in G2/M phase; On the other hand, Disitamab, a HER2 antibody, activates the cGAS-STING signaling pathway and increases IFN-β secretion, which can promote immune cell infiltration, enhance anti-tumor immunity, and improve the cytotoxic of tumor-infiltrating lymphocytes. Here, CGAS is linked to colonic neoplasm.