Moreover, in murine colitis and colorectal cancer models, ILC3s exhibit increased phenotypic plasticity and transited to ex-ILC3s (RORγt− ILC3s) or ILC1s driven by IL-23 and transforming growth factor β (TGF-β) in the induced lymphoid follicles, which are ILFs-like tissues termed ‘tertiary lymphoid structure’ [27]. This evidence concerns the gene TGFB1 and colorectal cancer.