The gastric hormone gastrin stimulates gastric acid secretion and epithelial cell proliferation. Multiple active products are generated from the precursor, preprogastrin, including the well-characterized amidated gastrins acting at the cholecystokinin-2 (CCK-2, or gastrin-CCK(B)) receptor, and others that may be growth factors in a range of cancers. Plasma concentrations of the amidated gastrins are elevated as a consequence of gastrin-secreting tumours (gastrinomas) and in conditions in which the normal inhibition of the antral G-cell by acid is depressed, for example chronic atrophic gastritis and prolonged treatment with proton pump inhibitors. There may also be increased gastrin release in Helicobacter pylori infection. Provocative tests for the diagnosis of gastrinoma include the secretin and calcium infusion tests. Hypergastrinaemia is associated with enterochromaffin-like (ECL) cell proliferation; the factors that determine progression to ECL cell dysplasia and gastric ECL cell carcinoid tumours are discussed. Several strategies for inhibiting the effects of gastrin are under evaluation, and their potential application is discussed.