Given the importance of Th17 cells in autoimmunity [37], the differential genetic effects observed in various autoimmune phenotypes mediated by the IL23R and KIAA1109-TENR-IL2-IL21 regions, evidence for genetic interaction between the KIAA1109-TENR-IL2-IL21 region and IL23R (in ulcerative colitis at least) [38], there are reasonable grounds for considering the hypothesis that genetic control of the Th1/Th17 axis is centered on cytokines (and their receptors) important in Th17 biology. This evidence concerns the gene IL21 and ulcerative colitis.