Following epithelial barrier disruption caused by DSS administration, IL-33 injection worsened colitis, inducing the recruitment of neutrophils to the site of inflammation41–43 and induction of type 2 cytokines44–46, whereas, during the recovery phase, it showed a prominent effect in promoting mucosal healing41, 43 and inducing goblet cell proliferation42, eventually restoring epithelial barrier function. The gene discussed is IL33; the disease is colitis.