VIPR2 and Hepatic steatosis: Although IL-22 within the intestinal environment can be produced by various immune cells, including T-helper type 17, T-helper type 22, γδ T cells, and innate lymphoid cells,12, 38, 39 the selective expression of VIPR2 in ILC318 and our results suggest that specific modulation of ILC3-derived IL-22 could be sufficient to attenuate the development of hepatic steatosis.