Taken together, substitution of MuSK-IgG for ColQ leads to enhanced suppression of MuSK signaling, as well as to lack of ColQ-mediated enhancement of membrane-bound MuSK, which are likely pathomechanisms underlying defective neuromuscular signal transmission in MuSK-MG model mice (Fig. 6). This evidence concerns the gene MUSK and myasthenia gravis.