STING1 and neoplasm: Upon activation by CDNs (e.g., cGAMP), STING triggers IFN‐I responses that further activate multifaceted downstream proinflammatory responses.[14] This allows the maturation of APCs to promote tumor antigen presentation and the priming of antitumor T cells.[15] Moreover, cGAS‐STING activation in the TME can also turn an immunosuppressive “cold” TME to a proinflammatory “hot” TME, the latter of which is critical for effective immunotherapy of solid tumors.