Boehringer Ingelheim reported discovery of small-molecule cGAS inhibitors with potential applications across autoinflammatory interferonopathies, idiopathic pulmonary fibrosis, metabolic-associated steatohepatitis (MASH) and systemic autoimmune disease. The disclosure details chemotypes and preclinical target engagement data. The study highlights biochemical potency, cellular cGAS–STING pathway suppression, and in vivo models showing reduced type I interferon signatures. Authors propose cGAS blockade as a way to dampen pathogenic innate immune activation without global immunosuppression. Clarification: cGAS is a cytosolic DNA sensor that triggers interferon responses; inhibiting cGAS can reduce chronic inflammatory signaling implicated in fibrotic and autoimmune disorders.