CXCL9 and neoplasm: Interestingly, we found that acetate upregulated the transcription and expression of GPR43, accompanied by an increase in the production of IFN-γ and IFN-γ-inducible CXCL9, CXCL10 and CXCL11, enhanced the infiltration of CD8+ T lymphocytes, and delayed tumorigenesis of OPC, suggesting that acetate generated by microorganisms could promote anti-tumor immunity to sufficiently improve the therapeutic efficacy.