The etiologic knowledge of myasthenia gravis is as yet incomplete, and the finger of suspicion is still directed at the endocrines. However, clinical insight relative to symptomatic therapy and diagnosis of this disease has progressed rapidly since 1934. RECENT ADVANCES PERTAINING TO ETIOLOGY In 1934 Nevin,1concerned with muscle chemistry in myasthenia gravis, concluded that the myoneural junction would be the location of clue to more lucid understanding of the etiology and treatment of the disease. The work of Dale and Feldberg2indicated that normal excitation transmission at the myoneural junction depends on the liberation of acetylcholine. The work of Pitfield3and of Simon4reported in 1935 and of Kennedy and Wolf5in 1937 seemed to incriminate the endocrines for the dysfunction of acetylcholine at the myoneural junction. It was found, for example, that insulin improved myasthenia as did ephedrine and epinephrine, whereas thyroid and