This was borne out of experiments with mice lacking the AHR pathway in IECs (VillinCreAhrfl/fl), which have a normal intestinal immune compartment and no impairment in IL-22 production, but nevertheless were as susceptible to infection with C. rodentium as mice with overactive CYP1A1 in IECs (VillinCreR26LSL-Cyp1a1). The gene discussed is CYP1A1; the disease is infection.