These results are consistent with the previous studies showing that tumor cells can develop multiple strategies to suppress the intrinsic cGAS‐STING signaling, e.g., downregulating STING expression or reducing sensitivity to dsDNA or cGAMP.[68, 69] Thus, it is challenging to induce STING activation and subsequent IFNβ production in cancer cells when the cGAMP level remains below a certain threshold.[70, 71]. The gene discussed is STING1; the disease is neoplasm.