Since the main driver of intestinal inflammation in the DSS model is the damage to the epithelial barrier lining the colon that allows intestinal microbiota into submucosal compartments [69], and since therapeutic effects were observed immediately upon CTBp administration, we concluded that CTBp’s protective efficacy in the DSS colitis models were attained by the induction of TGFβ-mediated colonic epithelial wound healing. This evidence concerns the gene TGFB1 and colitis.