Although it has been reported increased expression of IL-17A during IBD (Fujino et al., 2003) and both IL-17R-deficient mice in TNBS-induced colitis model (Zhang et al., 2006) as well as IL-17A-deficient mice in a DSS-induced colitis model (Ito et al., 2008) were reported to worsen the clinical disease symptoms, some other opposing studies highlighted the protective role of IL-17A production in vivo (Ogawa et al., 2004; O'Connor et al., 2009). The gene discussed is IL17A; the disease is inflammatory bowel disease.