Moreover, IL-33 mainly localizes to the nucleus, but under appropriate signal stimulation such as inflammation, IL-33 is in response processed and passively released from necrotic cells or actively secreted into the extracellular milieu [5] and functions through binding to its receptor ST2 as a proinflammatory cytokine that participates in the development and progression of many diseases, including collagen-induced arthritis [6, 7], anaphylactic shock [8], inflammatory bowel disease [9, 10], autoimmune hepatitis, and ischemia reperfusion injury [11–13]. This evidence concerns the gene IL33 and autoimmune hepatitis.