We previously found that ICT-driven induction of iNOS+ macrophages was dependent upon IFN-γ, whereas ICT-driven depletion of CX3CR1+CD206+ macrophages was partially independent of IFN-γ.22 In our vaccine setting, we hypothesize that T cell-derived IFN-γ and other factors drive monocyte polarization to iNOS+ macrophages upon entering the tumor, but other signals promote CX3CR1+CD206+ macrophages as well. The gene discussed is IFNG; the disease is neoplasm.