Specifically regarding MC activity, patients with UC were found to have greatly enhanced IL-33 expression, and IL-33 producing myofibroblasts were a primary source of IL-33 in these ulcerative lesions and synergized with TGF-β to induce further myofibroblast differentiation; such cells were nearly absent in patients with Crohn’s disease [41]. The gene discussed is IL33; the disease is Crohn disease.