In conclusion, our findings suggest that downregulation of the CCL2/CCR2 and CXCL10/CXCR3 axes via inhibition of the NF-κB pathway in the tumor and the tumor microenvironment might have contributed to the antitumor effects of celecoxib observed in the mouse glioma model. The gene discussed is CXCL10; the disease is neoplasm.