Myasthenia gravis is an autoimmune disease. It has been found that the serum of patients with myasthenia gravis contains an anti-acetylcholine receptor antibody, which is produced in large quantities in the thymus due to chronic and persistent viral infection of the thymus (thymitis) or harmful substances. This antibody plays an important role in the pathogenesis of myasthenia gravis, as it damages and reduces functional acetylcholine receptors, thereby disrupting neuromuscular transmission and causing muscle paralysis. We all know that human muscle movements are innervated by nerves. Ultrastructurally, each muscle bundle is connected to a nerve endings, and each connection is called a synapse (motor end plate), while each synapse against the muscle surface is called the postsynaptic membrane, which is richly distributed with acetylcholine receptors, used to receive the neurotransmitter acetylcholine, a key structure to make muscle movement. If the receptors are occupied by anti-acetylcholine receptor antibodies, they close the receptors to acetylcholine and destroy the receptors and the postsynaptic membranes that surround them. As the disease progresses, the number of destroyed receptors and postsynaptic membranes gradually increases, the number of functional acetylcholine receptors decreases, and the conduction between nerves and muscles is impaired, resulting in muscle paralysis and worsening symptoms of myasthenia gravis. The cause of symptom relief after thymectomy excludes the following sources: 1. acetylcholine antigen; 2. production of antibodies to acetylcholine receptors; 3. direct attack on sensitized T-killer cells at the neuromuscular junction; 4. T helper cells that contribute to the production of antibodies to peripheral lymphocytes that have been sensitized; 5. thymic factors that activate the complement pathway leading to complement-mediated lysis.