Following epithelial barrier disruption caused by DSS administration, IL-33 appeared to worsen colitis, inducing the recruitment of neutrophils to the site of inflammation [59]–[61], whereas, during the recovery phase, IL-33 showed a prominent effect in promoting mucosal healing [59], [61] and inducing goblet cell proliferation [60], eventually restoring epithelial barrier function. This evidence concerns the gene IL33 and colitis.