The reason for the different response to RTX between AChR- and MuSK-MG patients is likely related to the different type of autoantibody-producing cells in the two disease subgroups: as reported above, autoantibodies against MuSK are produced by short-lived plasmablasts that are continuously regenerated from autoreactive CD20-positive B cells, thus depletion of these cells may be effective; autoantibodies against AChR likely derive from long-lived plasma cells, and hence total circulating IgGs remain constant in the long-term after CD20 depletion therapy (53, 54, 62). The gene discussed is MUSK; the disease is myasthenia gravis.