These limitations in specificity and efficiency of CD25-targeted interference with Foxp3+ Treg cell activity may account for the largely contradictory range of data in the NOD model, including precipitation of overt diabetes (16–19), accelerated diabetes progression in young but not adult mice (20), as well as maintenance of β cell tolerance (21–23), or even delayed onset of diabetes (22). The gene discussed is FOXP3; the disease is diabetes mellitus.