With this design, MAPN achieved the site‐specific release of KLA and CVR in response to the high levels of H2O2 in TME and intracellular GSH, activating the cGAS‐STING pathway and blocking the PD‐1/PD‐L1 pathway, ultimately initiating robust and durable T cell anti‐tumor immunity to inhibit the growth, recurrence, and metastasis of malignant tumors. The gene discussed is CGAS; the disease is neoplasm.