In the T-cell transfer colitis model, both Th1 and Th17 effector T-cell responses contributed to colonic inflammation.32–34 In contrast, adoptive transfer of Tregs could protect recipient mice from colonic inflammation.35 Recent results from mouse models of IBD suggested that T cell plasticity, in particular, the Th17-Treg axis, plays an important role in regulating immune responses in the intestines.31 These findings suggest that TRAIL may also have a role in regulating proinflammatory T cells and Tregs. The gene discussed is TNFSF10; the disease is colitis.