A rat study reports that gene silencing of complement C3 using GalNAc-targeted siRNA nearly eliminated plasma complement, preserved acetylcholine receptor levels, and reduced muscle weakness in a myasthenia gravis model. The approach targets a downstream immune effector rather than neuromuscular signaling directly. The results add complement blockade to the expanding toolkit for antibody-mediated neuromuscular disease, with GalNAc delivery suggesting a pathway to liver-dominant systemic exposure. The key question for translation will be durability, dosing, and safety across longer intervention windows.