IL-33/IL-1F11 is an important mediator for the development of Th2-driven inflammatory disorders and has also been implicated in the pathogenesis of GI-related cancers, including gastric carcinoma. We therefore sought to mechanistically determine IL-33’s potential role as a critical factor linking chronic inflammation and gastric carcinogenesis using gastritis-prone SAMP1/YitFc (SAMP) mice