STING1 and systemic lupus erythematosus: These suggest that IFIT3 may contribute to the overactivation of cGAS-STING signaling pathway in monocytes of human SLE, laying the foundation for IFIT3 to be a new therapeutic candidate for blocking type I IFN and other proinflammatory cytokines generation via the cGAS-STING signaling pathway in SLE patients (88).