A putative role for IL‐17 signalling in CD fibrosis is supported by the finding that an anti‐IL‐17 antibody can diminish colitis and fibrosis in the TNBS murine model through downregulation of collagen expression and pro‐fibrogenic cytokines such as IL‐1β, TGF‐β1, and TNF‐α,51 or possibly by reducing EMT.52 This evidence concerns the gene IL17A and colitis.