Consistent with these findings, adoptive transfer studies have demonstrated that cigarette smoke exposure selectively enhances the proinflammatory properties of Th17 cells and the immunosuppressive activity of Treg cells through a GPR15-dependent mechanism, underscoring GPR15 as a central regulator of divergent T-cell–mediated immune responses to environmental factors in colitis. The gene discussed is GPR15; the disease is colitis.