It is reported that the activation of STING in cancer cells does not contribute to the therapeutic effect, but the tumor tissues can produce CDN that transfers to tumor‐associated DCs and macrophages, and induces the production of IFN‐I, thereby activating the STING pathway of host immune cells.[6] It is also reported that the signal of STING in tumor cells is inhibited due to epigenetic silencing or missense mutations of STING or its upstream regulator cGAS.[8] However, when the tumor also expresses STING, all CDN‐based and non‐nucleotide STING agonists can yield optimal outcomes. Here, CGAS is linked to neoplasm.