IL17A and Hepatic fibrosis: Interestingly, TGFβ in the environment supports the expansion of KLRG1− ILC2 (which responds to IL‐33), instead of KLRG1+ ILC2 (which responds to IL‐25), leading to diminished IL‐10 production by ILC2 and increased myofibroblasts differentiation.[164] Further, an IL‐5+ ILC2 niche sustained by IL‐33high adventitial fibroblasts restrains IL‐17‐mediated liver fibrosis.[169] These results suggest the profibrotic role of KLRG1− ILC2 and the anti‐fibrotic role of IL‐5+ ILC2; while, further exploration is needed regarding the heterogeneity of ILC2.