The reversal of inflammation was not a simple diversion of a large number of pro-inflammatory effector T cells into Treg cells because indistinguishable fatal autoimmunity observed in Foxp3-deficient mice harboring Treg “wannabes” and Foxp3DTR neonates subjected to chronic ablation of Treg cells suggests that Treg “wannabes” do not provide notable non-redundant contribution to the disease progression5, 8, 13. Here, FOXP3 is linked to Autoimmunity.