The ability of the gastric hormone gastrin to stimulate gut epithelial cell proliferation has been appreciated since the late 1960s.1 However, aside from the special case of gastric carcinoid tumours arising from enterochromaffin-like cells, the contribution of gastrin to gastrointestinal neoplasia has been uncertain. Several developments now suggest a role for gastrin in both gastric and colorectal cancer. In the case of gastric cancer, recent evidence indicates a synergy between gastrin andHelicobacter infection in accelerating progression to atrophy and cancer.2 Different issues are involved in colorectal cancer. The important emerging concepts here are that (a) the gastrin gene is expressed in colorectal cancer cells, but (b) the main products of gene expression in these cells are not ligands for the gastrin-cholesystokinin receptor B (CCKB), although (c) they do act as colon growth factors. The paper by Smith and Watson3 now shows that gastrin mRNA, detected by reverse transcription-polymerase chain reaction, is expressed in early stage polyps, that the main forms of gastrin detected by immunohistochemistry are biosynthetic precursor peptides, and that there is also parallel expression of the …