In conclusion, lack of efficacy of ARGX-119 observed with three of our MuSK MG patient IgG4s in the MuSK MG passive transfer mouse models could not be explained by direct competition for binding with ARGX-119, but rather seems related to a fraction of (IgG4) MuSK (bivalent) antibodies which are capable of inducing significant amounts of MuSK phosphorylation present in some patient materials, which warrants further investigations. This evidence concerns the gene MUSK and myasthenia gravis.