In 2018, IFIT3 was found to be one of the genes that contribute to the overactive cGAS-STING signaling pathway in SLE monocytes, indicating that IFIT3 may serve as a therapeutic target to block the production of IFN and other proinflammatory cytokines generated by the cGAS-STING signaling pathway (35). This evidence concerns the gene IFNA1 and systemic lupus erythematosus.