A preclinical rat study reports that GalNAc-targeted siRNA silencing of hepatic complement C3 nearly eliminated plasma complement and preserved acetylcholine receptors while reducing muscle weakness in a myasthenia gravis model. The strategy leverages liver-targeted RNA interference to reduce a key effector pathway upstream of neuromuscular damage. The results position complement C3 as a tractable target and support further development of RNAi platforms that modulate systemic immunity with tissue-directed delivery.