In spite of the well-documented reports that administration of corticotropin (ACTH) stimulates the gastric secretion of acid and pepsin and may be complicated by the development or reactivation of peptic ulcer,1it does not necessarily follow that the increased secretion is the cause of the ulceration. The possibility, therefore, still exists that while adrenal stimulation by corticotropin undoubtedly can produce an increased secretion of acid and pepsin, it may also in some way interfere with the natural defenses of the gastric and duodenal mucosa against the digestive action of the gastric juices. The hypothesis that increased secretion of acid and pepsin is the cause of ulcers rests largely upon indirect evidence, such as the presence of increased gastric secretion of