Purpose: According to the recent studies, it is shown that the polymorphism of Interleukin $1eta$ gene is associated with the incidence of gastric cancer caused by the Helicobacter pylori infection. Interleukin $1eta$ is a cytokine markedly inhibiting gastric acid secretion. Interleukin $1eta$ production associated with Helicobacter pylori gastric infection may exacerbate mucosal damage including chronic gastritis and atrophic gastritis, may induce eventual neoplasia. Among these Interleukin $1eta$ gene polymorphisms, polymorphisms at -31 portion and -511 portion may associated with these processes, eventually increase the risk of gastric cancer. We investigated the risk of gastric cancer according to the Helicobacter pylori infection and genetic polymorphism of Interleukin $1eta$ in gastric cancer patients. Materials and Methods: 176 individuals with gastric cancer and 40 healthy controls were analyzed. Each group was divided into two groups whether they infected with Helicobacter pylori or not. DNA was extracted from the peripheral blood in all groups. The PCR-RFLP method was used for investigating the distribution of genotype of C/C, C/T, T/T at -31 portion and -511 portion. Results: T/T genotype at -511 portion was $19.3\%$ in gastric cancer cases and $10\%$ in controls, which was statistically significant. (P=0.0432) The risk of gastric cancer was increased 4.86 ($1.26∼18.77$) in group which had T/T genotype. In gastric cancer cases, C/C genotype at 31 portion was $27.6\%$ in group with Helicobacter pylori infection and $12.8\%$ in group without infection, which was statistically significant. (P=0.0047) The risk of gastric cancer was increased 4.82 ($1.81~12.81$) in group which had C/C genotype. Conclusion: T genotype at -511 portion among the Interleukin $1eta$ genetic polymorphisms may be the risk factor of gastric cancer. And, with Helicobacter pylori infection, C genotype at -31 portion may be the risk factor of gastric cancer.