Accumulating evidence shows that Th17 cells in inflammatory conditions are highly plastic and can transdifferentiate to IL-17/IFN-γ double-producing cells and Th1-like IFN-γ+ ex-Th17 lymphocytes (non-classic Th1), which seem to be more pathogenic than the unshifted cells in animal models of IBD [145,146]. Here, IL17A is linked to inflammatory bowel disease.