The provision of IFN-I by T cells in the context of cancer may be particularly important because STING signaling is suppressed in many tumors due to loss-of-function mutations or epigenetic silencing of the STING/cGAS promoter regions [60], and pDCs are reportedly defective in IFN-I production and physically colocalize with Tregs in the TME [61, 62]. Here, CGAS is linked to cancer.