Pre-cancerous inflammation is well established in the pathogenesis of gastric cancer, however the individual molecular pathways involved in this process are yet to be fully elucidated. Individually, both the potent pro-inflammatory cytokine IL-1β and the oncogenic latent transcription factor STAT3 are known to play a role in the development of gastric cancer. Using a STAT3-driven preclinical mouse model for gastric tumourigenesis (gp130^F/F), human gastric cancer specimens and in vitro techniques, we have established a link between STAT3-driven tumour burden and the inflammasome, the latter representing a multi-protein inflammatory complex that controls the production of mature, biologically-active forms of IL-1β (and IL-18). The effector molecules of inflammasome activation, namely activated caspase-1, IL-1β and IL-18 proteins, are upregulated in STAT3-driven gastric tumours. Genetic ablation of the inflammasome adaptor ASC reduced tumour burden by up to 50%, independent of inflammation and tumour cell proliferation. Rather, we have determined that the suppressed tumourigenesis is associated with increased tumour (epithelial) cell apoptosis in gp130^F/F mice null for the Asc gene. Furthermore, using bone marrow chimeras we have shown that the reliance on ASC for gastric tumourigenesis is independent of bone marrow-derived hematopoietic (immune) cells expressing ASC. Finally, in tumours from gp130^F/F mice, as well as in human gastric tumour biopsies, the expression of specific inflammasome-activating pattern recognition receptors are elevated. Overall, our results uncover a role for the inflammasome in the development of gastric cancer.