CGAS and Aicardi-Goutieres syndrome: The team also found that in the cells of patients with AGS as well as in mouse models, aspirin acetylated lysine residues (Lys384, Lys394, and Lys414) at positions 384, 394, and 414, respectively, of cGAS, which kept the cGAS protein inactive, prevented cGAS from activating downstream signaling pathways, and inhibited autoimmune responses (103).