Choline acetyltransferase, acetylcholinesterase, and pseudocholinesterase levels were measured in needle biopsy samples of deltoid muscle from subjects with myasthenia gravis and from normal controls. Choline acetyltransferase activities were about 30% lower and acetylcholinesterase activities about 45% lower in myasthenics as compared with controls. These decreased activities, however, are not significant in the cause of the disease; it is postulated that the primary defect at the neuromuscular junction may be the presence of a false transmitter in the synaptic vesicle or defective release of the vesicle contents at the synaptic cleft.