Taken together, over-activation (high KYN/TRP) of the KP, up-regulated IDO-1 expression, and enhanced TRP catabolism in glioma cells in response to IFN-γ and the IDO-1 over- expression in glioma cells is likely to play a role in mediating brain tumor immune evasion via inhibiting tumor-specific immunity and driving malignant progression. The gene discussed is IFNG; the disease is central nervous system cancer.