Treatment of acute exacerbations and refractory myasthenia gravis (MG) remains challenging despite advances in immunotherapy. Frequent use of plasmapheresis and immunoglobulins are associated with adverse events and strain on resources. The neonatal Fc receptor (FcRn) facilitates IgG recycling and FcRn antagonism enhances the degradation of IgG pathogenic autoantibodies without compromising adaptive and innate immunity. Efgartigimod, an FcRN antagonist, has been shown in well-designed clinical trials to improve clinical status and reduce autoantibody levels without significant safety concerns. Efgartigimod has received approvals for use in the United States, Japan and Europe. It is plausible that efgartigimod is effective across different subgroups and varied spectrums of MG severity. Novel strategies involving FcRn modulation and long-term follow-up studies will help provide further insights and expand the therapeutic repertoire.