Type 3 inflammation, characterized by a polarization towards a Th17 response and the production of IL-17A, IL-17F, IL-22 and IL-26 by Th17 cells, Th 22 cells, neutrophils and mast cells has been identified as a driver of chronical liver injury and of TGF-β-dependent liver fibrosis [73]. This evidence concerns the gene IL17A and Hepatic fibrosis.