The only gastrin-dependent gastric endocrine cells are the fundic ECL cells. Excessive hypergastrinemia stimulates ECL cell proliferation in animals and man. The growth of other gastric endocrine cells is regulated by the gastric pH. Hypergastrinemia in man results in diffuse and linear hyperplasia of the ECL cells, while micronodular hyperplasia is correlated to the grade of corpus gastritis. ECL cell dysplasia and gastric carcinoids in man have been observed only in patients with gastrinoma as part of the MEN I syndrome and with pernicious anemia. Gastrin dependence of GI adenocarcinoma has not been established. Experimental findings may be explained by the presence of gastrin receptors and the role of gastrin as an autocrine growth factor. Epidemiological data do not support gastrin dependence of carcinoma of the stomach, the pancreas and the colon.