Moreover, because colonic polyps are characterized as a transition state of the progression from normal epithelial cells to cancerous cells where EMT is critical to this progression, Jak3 acts as a critical regulator of uncontrolled epithelial proliferation (and hence the formation of colonic polyps) by suppressing EMT following successful mucosal wound repair and promoting mesenchymal-epithelial transition (MET). Here, JAK3 is linked to colon inflammatory polyp.