The reported delay and lower incidence of diabetes development in NOD mice treated at 2–3 weeks of age with an anti-IFN-AR1 mAb (13), together with the reversibility of IL-10 signaling inhibition we observed in vitro in T cells after removing IFN-β, are encouraging indications that the unbalanced immune regulation of NOD mice can be prevented or restored. Here, IFNA1 is linked to diabetes mellitus.