IFNγ may promote tumor metastasis by inducing the upregulation of ICAM1, CD133, and CXCR4, and the production of MUC4, as well as promoting EMT.42,43 IFNγ may also increase indoleamine-2,3-dioxygenase (IDO), CTLA4, and PD-L1 production, thus mediating tumor immune escape.44,45 In the current study, we provide a novel mechanism involved in its pro-tumor effects, whereby PA stimulates Vγ9Vδ2-T cells to secret an excessive amount of IFNγ, which further induces Vγ9Vδ2-T cell pyroptosis and impairs their function and metabolism, ultimately leading to the loss of their antitumor activity. The gene discussed is MUC4; the disease is neoplasm.