In our pre-clinical model, Tregs seem to play a major role in mediating B16IDO tumor progression given that the selective depletion of Tregs, using a transgenic mouse strain engineered with a transgene that expresses the diphtheria toxin receptor (DTR) under control of the Foxp3 promoter (Foxp3DTR mice), led to regression of B16IDO tumor growth (Fig. 3b). This evidence concerns the gene FOXP3 and neoplasm.