The clinical relevance of these findings is substantiated by previous data demonstrating that IBD is characterized by increased expression of innate (IL-12, IL-23) and adaptive (IFN-γ, IL-17) proinflammatory cytokines [5], and Th1, Th17 polarization is mainly controlled by the IL-12p70 and IL-23 cytokine family produced by activated DCs [49]. The gene discussed is IL23A; the disease is inflammatory bowel disease.