In particular, studies investigating IL-33 in gut inflammation could show that recombinant IL-33 treatment resulted in an improved outcome of experimental intestinal inflammation in mice through the activation of ILC2s in an AREG-dependent manner or through the induction of CD103+ DCs to promote the development of Tregs via IL-2 secretion (25, 39, 40). The gene discussed is IL33; the disease is inflammation.