Although several cGAS inhibitors have been reported recently, few inhibitors have been tested in autoimmune mouse models in vivo,44,45 except for the antimalarial drug derivative X6, which attenuated the autoimmune disease phenotype in Trex1−/− mice.30 Numerous posttranslational modifications have been shown to play important roles in regulating the DNA-sensing ability or enzymatic activity of cGAS,15,16,46,47 but chemicals that can specifically/effectively alter these modifications have rarely been identified to date. Here, CGAS is linked to autoimmune disease.