Carcinogenesis is a highly complex process involving both inherited risk factors and environmental ones such as diet, smoking, occupation, and exposure to radiation and chemical agents. Experimental toxicology identifies potentially carcinogenic chemicals and thus makes it possible to introduce regulatory measures aimed at reducing human exposure to them. Carcinogenesis can be viewed as consisting of three distinct sequences: initiation, promotion, and progression. Neoplastic conversion (initiation) occurs when a genetic event (e.g., point mutations, chromosomal rearrangements, insertion or deletion of genes, and gene amplification) results in oncogene activation and/or lack of expression - or inactivation of products - of tumor suppressor genes. Promotion involves clonal expansion of initiated cells and requires cell proliferation. Effective strategies for reducing risk of gastric cancer or neoplasias at other sites should include both control of known carcinogens and chemical prevention through rational interventions in the carcinogenic process. The toxicologist's challenge is thus to devise better and less expensive predictive assays and to elucidate the mechanisms underlying chemical carcinogenesis.