['Gastric carcinoids are slow growing neuroendocrine tumours arising from enterochromaffin-like (ECL) cells in the corpus of stomach. Although most of these tumours arise in the setting of gastric atrophy and hypergastrinemia, it is not understood what genetic background predisposes development of these ECL derived tumours. Moreover, diffuse microcarcinoids in the mucosa can lead to a field effect and limit successful endoscopic removal.', 'To define the genetic background that creates a permissive environment for gastric carcinoids using transgenic mouse lines.', 'The multiple endocrine neoplasia 1 gene locus (Men1) was deleted using Cre recombinase expressed from the Villin promoter (Villin-Cre) and was placed on a somatostatin null genetic background. These transgenic mice received omeprazole-laced chow for 6\u2005months. The direct effect of gastrin and the gastrin receptor antagonist YM022 on expression and phosphorylation of the cyclin inhibitor p27', 'The combination of conditional Men1 deletion in the absence of somatostatin led to the development of gastric carcinoids within 2\u2005years. Suppression of acid secretion by omeprazole accelerated the timeline of carcinoid development to 6\u2005months in the absence of significant parietal cell atrophy. Carcinoids were associated with hypergastrinemia, and correlated with increased Cckbr expression and nuclear export of p27'] Does deletion of Men1 and somatostatin induce hypergastrinemia and gastric carcinoids?