The absence of ILC1s in T-bet−/− mice is linked to increased susceptibility to enteric infections.2,6,12–14 We have previously reported the phenotype of TRUC mice that develop spontaneous colitis, which is dependent on IL-17-producing CCR6+ ILC3s in the absence of adaptive immunity.5 Increased frequency of inflammatory ILC1s has also been found in inflamed intestine from Crohn’s disease patients.6,13,15 However, whether T-bet expression in ILCs drives protective or pathogenic mucosal immune responses in the presence of an intact immune system still needs to be elucidated. This evidence concerns the gene IL17A and colitis.