HBEGF and neoplasm: 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).