A series of 30 gastric endocrine tumours has been revised in the light of available available cytologic and clinicopathologic information. Among 24 well differentiated endocrine tumours-16 with and 8 without chronic atrophic gastritis (CAG)-3 gastrin cell tumours have been distinguished from 21 argyrophil carcinoids, 15 of which showed light- and/or electronmicroscopy patterns of enterochromaffin-like (ECL) cell tumours, 2 of EC cell tumours and 1 of D1/P cell tumour. One case of mixed carcinoid/adenocarcinoma and 5 cases of endocrine carcinomas, 4 poorly and 1 moderately differentiated, were also identified. Achlorhydria, due to type A CAG or HCl-suppressing drugs, and bombesin hyperstimulation are among possible factors inducing G cell hyperfunction and/or hyperplasia. Hypergastrinaemia is among causative agents of argyrophil ECL cell hyperplasias and, possibly, of tumours of the oxynticopeptic mucosa, while chronic inflammation and gland atrophy with or without concomitant hypergastrinaemia are important factors in inducing both hyperplastic and tumour argyrophil growths in CAG mucosa.