The dual observations (see above) of (1) the ability of IgG isolated from patient serum, when injected into immunosuppressed mice, to induce a disease similar to human MuSK-MG, and (2) immunization of normal animals with purified MuSK protein, leading to the production of MuSK Abs, also results in a disease that is highly similar to human MuSK-MG, together strongly support the hypothesis that the MuSK Abs are the etiologic agents in this disease. The gene discussed is MUSK; the disease is myasthenia gravis.