In the present study, we used Foxp3 (forkhead box P3) transgenic mice expressing the diphtheria toxin (DT) receptor under the control of the Foxp3 promoter, which made it possible to selectively deplete Tregs in vivo and to determine the influence of Foxp3+ Tregs on T-cell responses during tumor regression. This evidence concerns the gene FOXP3 and neoplasm.