AGRN and myasthenia gravis: As known from previous studies, MuSK-IgG4 antibodies undergo Fab-arm exchange in vivo becoming functionally monovalent, and their Fab fragments inhibit agrin-induced MuSK phosphorylation and AChR clustering.9,10 Recent studies have used engineered monovalent or divalent monoclonal antibodies, derived from MuSK-MG patient B cells, to explore the roles of subclass and valency.