Considering that Th17 cells have been demonstrated to be pivot cells in pathogenicity of HSD in encephalomyelitis (5, 6) as well as colitis (12–14) models, that ILC3 are very abundant in the gut mucosa and that they are increased in the colon of individuals during the course of IBD (17, 18), it is likely that the effect of HSDs in colitis development is dependent on IL-17 production by both Th17 cells and ILC3. Here, IL17A is linked to colitis.