In fact, as opposed to their results obtained from IL-33 treatment in acute DSS colitis, Groβ et al. showed that IL-33 administration during repeated, chronic cycling of DSS causes a reduction of colitis, suppresses IFNγ, and decreases bacterial translocation (176), supporting a protective role of IL-33 that the authors suggest may occur by switching from Th1- to Th2-driven immune responses. The gene discussed is IL33; the disease is colitis.