Although retained AChE and AChR in biopsied muscles in MuSK-MG patients cannot explain compromised neuromuscular signal transmission especially in bulbar muscles, heterologous overexpression of recombinant ColQ, or of recombinant CTD may partially ameliorate defective neuromuscular signal transmission caused by MuSK-IgG. This evidence concerns the gene MUSK and myasthenia gravis.