GAST and gastric carcinoma: To our knowledge, our explanation of the role of gastrin in stimulating the ECL cell directly and thereby predisposing patients to gastric carcinomas of the diffuse type, and the stem cell via the stimulation of the release of mediators from the ECL cell leading to gastric carcinomas of the intestinal type, is presently the only plausible theory of gastric carcinogenesis secondary to oxyntic atrophy (Figure 2) [123,124].