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The spectrum of autoantibodies present in patients with acquired autoimmune myasthenia gravis (MG) has expanded significantly in the last decade. The nicotinic acetylcholine receptor (nAChR) is the most frequent (and well-known) antigenic target of the autoimmune response in MG, followed by antibodies directed against muscle-specific tyrosine kinase (MuSK). A small proportion of double (nAChR and MuSK) seronegative patients possess antibodies that target low-density lipoprotein receptor-related protein 4 (LRP4). Building on the observation that MG can be caused by autoantibodies that directly bind to the nAChR or to proteins (MuSK and LRP4) that mediate nAChR aggregation at the neuromuscular junction, investigators have now sought evidence …