Similarly, in a mouse model of MuSK-MG, obtained by injections with purified MuSK-MG patients’ IgG4, FcRn blockade by efgartigimod reduced IgG4 levels and determined significant in vivo muscle function improvements, thus highlighting the potential of FcRn-targeted therapies to effectively improve MG (90). The gene discussed is FCGRT; the disease is myasthenia gravis.