In orthotopic, immunocompetent transplant models and in genetically engineered mouse models, the BiTE exhibited a two-pronged activation mechanism: selective engagement of IL-13Rα2+ tumor cells and CD3-dependent release of IFN-γ and tumor necrosis factor-α (TNF-α), together with GZMB-mediated cytotoxicity. The gene discussed is GZMB; the disease is neoplasm.