Interestingly, the lower percentages of CD4+ Tregs in NOD mice are not due to differences in persistence, survival, or homeostatic proliferation of CD4+Foxp3+ or CD4+Foxp3− cells in NOD compared to B6 (non-T1D-prone strain) mice but do seem to be due to a considerably higher rate of thymic export of CD4+Foxp3− cells in NOD mice that was first observed shortly before disease onset (i.e., ~13-15 weeks) at 9-10 weeks of age. This evidence concerns the gene FOXP3 and type 1 diabetes mellitus.