Myasthenia gravis (MG) is an autoimmune disease caused by antibodies mainly directed to the acetylcholine receptor (AChR) of the neuromuscular junction. Induction of antigenic modulation and complement activation by such autoantibodies leads to ultrastructural damage of the postsynaptic membrane and loss of AChR and associated proteins. Reduction of antigenic modulation by increasing the expression of the receptor-associated anchor protein, rapsyn, or by functionally monovalent competing IgG4 anti-AChR antibodies was shown to prevent MG disease activity. We propose that preventing antigenic modulation can be used as a treatment strategy for MG.