Maintenance of the NMJ does appear to require MuSK functionality, as demonstrated by the dissolution of the synapse in adult animals (in the absence of inflammation) both in (1) experimental MuSK-MG induced by either passive or active immunization with MuSK (59–63) and (2) in adult animals in which MuSK has been inactivated or knocked down (64, 65). This evidence concerns the gene MUSK and myasthenia gravis.