Studies in the nonobese diabetic (NOD) model of spontaneous T1D demonstrated that the administration of low-dose IL-2 rescues islet Tregs by supporting the expression of the antiapoptotic B-cell leukemia/lymphoma 2 protein, promoting their local proliferation, and enhancing their suppressive capacity (14, 15). The gene discussed is IL2; the disease is type 1 diabetes mellitus.