Autoimmune diseases in Trex-1 and DNase II-deficient mice were shown to be dependent on the cGAS-STING pathway (45, 46), and other murine studies have demonstrated the contribution of the cGAS-STING pathway to enhancing type I IFN responses in lupus or lupus-like mouse models (47–49). This evidence concerns the gene STING1 and autoimmune disease.