IL-2 can induce Tbet and IL-12Rβ2 and promote TH1 differentiation with enhanced IFN-γ production (67), indicating a mechanism for how increased IL-2 signaling may enhance IFN-γ production in Treg cells and limit their suppressive function, observations that support the idea that IFN-γ derived from BLIMP1-deficient Treg cells may contribute to inflammation in colitis and possibly in other autoimmune conditions. The gene discussed is PRDM1; the disease is colitis.