While the molecular basis underlying these processes remains unclear, previous studies have shown that administration of the AhR agonist, FICZ, ameliorated colitis severity by downregulating pro-inflammatory cytokines and upregulating IL-22 production in DSS-, 2,6,4-trinitrobenzene sulfonic acid (TNBS)-, and T-cell transfer-induced colitis 34. The gene discussed is IL22; the disease is colitis.