Myasthenia gravis (MG) stands as an autoimmune neurological disorder characterized by impaired transmission at the neuromuscular junction. The incidence of MG ranges from 5.1 to 30 cases per million person-years, with a prevalence rate falling between 150 and 200 cases per million. MG serves as a classic illustration of antibody-mediated autoimmune disease, with a majority of patients exhibiting autoantibodies against acetylcholine receptors (Ach Rs). Other, less frequently observed autoantibodies target muscle-specific kinase (Mu SK), low-density lipoprotein receptor-related protein 4 (Lrp4), and agrin. These autoantibodies interfere with cholinergic transmission between nerve terminals and muscle fibers, leading to downregulation, destruction, functional blocking of Ach Rs, or disruption of AC hR clustering in the postsynaptic membrane. The primary clinical manifestation of MG is fatigable muscle weakness, impacting ocular, bulbar, respiratory, and limb muscles. The specific clinical presentation varies based on the type of autoantibody and the presence of a thymoma.