Mutations in genes that govern the assembly and maintenance of neuromuscular synapses, or mediate synaptic transmission, are responsible for congenital myasthenia, whereas autoantibodies to key postsynaptic proteins, such as AChRs and MuSK, are responsible for autoimmune myasthenia gravis (MG) (13, 14). This evidence concerns the gene MUSK and congenital myasthenic syndrome.