It is considered that about sixty-five percent of people are suffering from Helicobacter pylori infection in our country. In the East Asian countries including Japan, such fungus as aspergillus are ubiquitously found in the environment as a contaminant in human food stuffs and animal feeds. Sterigmatocystin is a mycotoxin and a precursor of aflatoxin which is produced by Aspergillus versicolor. The mechanisms of gastric carcinoma development induced by the combination of Helicobacter pylori infection with Sterigmatocystin, a mycotoxin are shown and discussed. We revealed that Sterigmatocystin-treated cells exhibited an absence of P53-mediated G1 arrest with induction of MDM2 at 12 and 24 hours of treating time. Furthermore, it was revealed that long term treatment with Sterigmatocystin enhanced dominantly the development of intestinal metaplasia, and of precancerous lesions of gastric mucosa in Helicobacter pylori-infected Mongolian gerbils. It has been reported that the accumulations of P53 nucleotide substitutions in the H. pylori-infected monkeys were increased as the score of gastric atrophy increased, nevertheless no mutations were noted in the H. pylori-uninfected monkeys. The mechanisms of the development of gastric cancer produced by combination of H.P. with ST remain to be unclear. Further study concerning the mechanisms must be carried out.