The pathogenesis of myasthenia gravis (MG) includes autoantibody attack on the AChR in the postsynaptic membrane at the muscle endplate site, suggesting that the first priority in the treatment of MG is to reduce this autoimmune attack. Thus, measures that directly target the abnormal autoimmune response are more effective treatments for patients with MG, and these treatments usually include two categories: those that have a rapid onset of action but a short duration of efficacy, and those that have a long-term therapeutic effect. Most current treatments for autoimmune diseases refer primarily to immunosuppressive drug therapies; therefore, therapeutic measures are often understood as the application of high doses of immunosuppressive drugs to bring the disease into remission, followed by a reduction to the smallest maintenance dose that can maintain symptomatic remission. In MG and most other autoimmune diseases, the taper of immunosuppressive drugs should be slow. Specific application needs to be individualized in relation to the patient’s condition, clinical staging, other systemic disease conditions, and previous sensitivity to different therapies.