Peptic ulcers of the stomach and duodenum look much alike and the reaction around them is nonspecific, yet other evidence indicates that ulcers in the two locations do not represent the same disease. It is suggested that a common causal factor is the digestive effect of gastric juice, and that hypersecretion may produce duodenal ulcer without any predisposing change in the relatively susceptible duodenum. The development of a gastric ulcer, which may occur without hypersecretion, presumably requires some previous alteration of the normally resistant gastric mucosa. Focal metaplasia of the gastric mucosa to tissue resembling the lining of the small intestine, which is observed frequently in association with gastric ulcer, may be a factor in providing decreased resistance to peptic injury.