The strong inverse correlation between CCR6+ Th17 cell abundance and histologic colitis (r = -0.946) points to a protective function of CCR6+ Th17 cells in the colonic mucosa, which is both consistent with the fact that Th17 cytokines enforce barrier function in the gut [16] and supported by previous data from both animal models of IBD and clinical trials; Th17 cells are capable of suppressing experimental colitis in mice [21], and the neutralizing IL-17A antibody, Secukinumab, not only failed to show efficacy in a recent IBD clinical trial, it exacerbated disease activity [22]. This evidence concerns the gene CCR6 and colitis.