Gastric cancer is the 3rd leading cause of cancer deaths worldwide. Over 90% of gastric cancers are associated with long-term Helicobacter pylori infection. However, the infection alone has limited pathogenic effects on the gastric mucosa. Rather, the infection triggers massive gastric inflammation, which becomes increasingly hyperactive, damaging the stomach and creating the requisite environment for carcinogenesis. However, the mechanisms and pathways that regulate the onset of hyperactive inflammation are unknown.