Overall, the general finding that attenuation of IFN-γ facilitates the production of CCL22 and results in recruitment of Treg cells to tumor sites, in turn resulting in additional inhibition on IFN-γ, leads us to speculate that the cyclic interaction between IFN-γ, CCL22, and Treg cells may comprise a positive feed-back mechanism for increasing the survival and malignancy of tumor cells. Here, IFNG is linked to neoplasm.