Although in vivo studies indicate that AhR−/− mice generate normal adaptive immune responses to model antigens (Vorderstrasse et al., 2001) and that AhR−/− donor CD4+ T-cells differentiate normally during an acute GVH response (Kerkvliet et al., 2002; Funatake et al., 2005), AhR-deficient mice have been reported to express a hypersensitive phenotype in experimental colitis, and following challenge with either LPS or cigarette smoke (Thatcher et al., 2007; Sekine et al., 2009; Furumatsu et al., 2011). The gene discussed is CD4; the disease is colitis.