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Abstract Whether cyclic GMP–AMP synthase (cGAS)–stimulator of interferon genes (STING) signaling should be inhibited in inflammatory bowel disease (IBD) cannot be answered from pathway abundance alone. Canonical ER–Golgi–TBK1–IRF3/NF-κB signaling can amplify intestinal inflammation, whereas nuclear STING–AHR signaling, T-cell-intrinsic STING, ILC3 sensing, and epithelial antimicrobial programs may support microbial tolerance, host defense, or repair.
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