Further evidence for involvement of the IL-33/ST2 axis in CRC pathogenesis comes from an inflammation-driven model in which ST2 deficiency in mice conferred protection against tumor development (61) and secondly from a polyposis mouse model (ApcMin/+), where abrogation of IL-33 signaling reduced the tumor burden, Th2-associated cytokine production and mast cell activation (59). The gene discussed is IL1RL1; the disease is polyposis.