These data together highlight a novel non-canonical function of ILC1 in the exacerbation of IBD, in which their augmented expansion may be coupled to enhanced TGF-β signaling, consequentially driving the inflamed tissues toward fibrotic scar tissue formation and/or promoting the growth of epithelial tumors during chronic inflammation, two life-threatening sequalae of IBD (74). This evidence concerns the gene TGFB1 and inflammatory bowel disease.