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Twenty years ago, the discovery of a deficit of acetylcholine receptors at the neuromuscular junctions of patients with myasthenia gravis1 and the development of an animal model of the disease2 shed new light on a disorder that was first described clinically 300 years earlier by the great physiologist Thomas Willis3. During the past two decades, remarkable progress has been made in our understanding of myasthenia gravis, and the new knowledge has been applied directly to the clinical diagnosis and treatment of this formerly grave disease. Myasthenia gravis is undoubtedly the most thoroughly understood of all human autoimmune diseases and . . .