Current data generated from two different mouse models support the hypothesis that IL-33 also contributes to the pathology of renal fibrosis: in unilateral ureteral obstruction (UUO), Chen et al. reported reduced parenchymal loss and enhanced epithelial proliferation in both IL-33- and ST2-deficient mice4, and in renal ischemia–reperfusion, Liang et al. showed that inhibition of IL-33 signaling by administration of soluble IL-33 receptor (sST2) also reduced fibrosis5. Here, IL33 is linked to renal fibrosis.