IL17A and colitis: This hinted that in the course of TNBS-induced colitis, activated PI3K/Akt signal pathway possibly heightened transcription of NF-κB, and then promoted to secrete proinflammatory cytokines (including IL-2, IL-6, IL-17, and IL-23), inhibited expressions of HSP70 and TGF-β, and finally led to inflammatory injury of colonic mucosa.