The first description of this came from studies in the TRUC mouse (T-bet−/− x RAG2−/− ulcerative colitis), which develop spontaneous colitis dependent on IL-17-producing ILC3s.5 Furthermore, within the CCR6− ILC3 subset, T-bet expression is required for CCR6-/low ILC3s differentiation into NCR+ ILC3s and subsequent IFNγ production.2,6,7T-bet is also induced in human and murine ILC2s, resulting in the production of IFNγ.8–11 Among several cytokines, IL-12 and IL-18 appear to be the main driver of these effects, however their pathophysiological relevance is still unknown. This evidence concerns the gene IFNG and colitis.