We reasoned that if diminished GRAIL expression leading to loss of inhibition of IL-2R desensitization was a common defect in mouse models of autoimmunity, where a defect in GRAIL expression had been identified (28), it might be possible to restore Treg function using low-dose IL-2 in combination with an NAEi in these mouse models of disease. The gene discussed is IL2RA; the disease is Autoimmunity.