In mice, Treg depletion impairs oral tolerance.1 Adoptively transferred Tregs prevent the onset of colitis or treat established colitis in a number of murine models.2–7FOXP3 mutations lead to multisystem autoimmunity with enteropathy in mice and humans.8, 9 Disruption of other key molecules implicated in Treg function, such as transforming growth factor (TGF)-β, Cytotoxic T Lymphocyte-Associated (CTLA)-4, interleukin (IL)-10R subunits, IL-2 or its receptor subunits, is associated with autoimmunity and intestinal inflammation.10 This evidence concerns the gene IL2 and colitis.