Gastric cancer remains a leading cause of cancer-related mortality worldwide, with limited therapeutic options for early intervention. Recent findings have uncovered a previously unrecognized pro-tumorigenic role for a conserved immune circuit involving epithelial tuft cells and type 2 innate lymphoid cells (ILC2s). Originally evolved to combat helminth infections, this IL25–IL13-driven signalling axis becomes hijacked in the gastric mucosa to promote metaplastic transformation and tumor development. Using genetically engineered mouse models and human gastric cancer datasets, we demonstrate that tuft cell-derived IL25 activates ILC2s, which in turn secrete IL13 to drive tuft cell hyperplasia—forming a feed-forward loop that sustains epithelial proliferation and tumor progression. Disruption of this circuit through genetic ablation or antibody-mediated blockade of IL25 or IL13 significantly reduces tumor burden and improves survival in preclinical models. Furthermore, co-expression of tuft cell and ILC2 gene signatures correlates with poor prognosis in patients with intestinal-type gastric cancer. These findings position the tuft cell–ILC2 axis as a novel and actionable therapeutic vulnerability in gastric cancer, with potential for rapid clinical translation using existing cytokine-targeting biologics.