BCL2L1 and colitis: The addition of exogenous IL-22 increased gene transcription levels of survival proteins (bcl-2, bcl-xL, mcl-1), anti-apoptotic molecules (c-myc, cyclind1, rb2, cdk4), and mucosal barrier protective molecules (mucin1, mucin2, mucin10), while the deletion of IL-22 significantly impaired tissue repair in DSS-induced colitis mice models, and no repair occurred after acute injury [46,47].