While Foxp3-deficient NOD mice failed to develop insulitis and overt diabetes (33), studies in Foxp3.CNS1–/– NOD mice have provided ambiguous results, providing evidence for either a dispensable (34) or nonredundant function (35) of Foxp3.CNS1-dependent pTreg cells in the control of destructive β cell autoimmunity. The gene discussed is TTC4; the disease is diabetes mellitus.