It is well accepted that the overproduction of proinflammatory cytokines (such as TNF-α, IL-1β, IL-6, IL-17α, and IFN-γ) causes serious tissue damage, enhances inflammatory reactions in human IBD, and is observed in chemically induced experimental rodent colitis models (including DSS- and TNBS-induced colitis) [3, 6, 7, 19]. The gene discussed is IL17A; the disease is colitis.