Collectively, these findings indicate that B16F10 tumor response to DCP-IL-12/FLT3L is strictly IFNγ-dependent, involves a diverse assortment of IFNγ-producing cells and may depend, at least in part, on the antitumoral activity of IFNγ-stimulated M1-like TAMs. This evidence concerns the gene FLT3LG and neoplasm.