IL-13 receptor alpha 2, also known as CD213α2, is a subunit of IL-13 receptor complex. It is encoded by the gene locus Xq13.1-q28 on chromosome X. An important characteristic of this subunit is that it does not have a cytoplasmic domain. Even though, the IL-13 Rα2 binds to IL 13 with high affinity, the receptor appears not directly involved with a typical IL-13 stimulated signal transduction. Unlike IL-13Ra1, the binding of IL-13Rα2 to IL-13 is IL-4R independent and is not associated with Jaks and the phosphorylation and activation of Stats. There are evidences that soluble IL-13Rα2 may serve as decoy receptor to dampen the cell reaction to IL-13 stimulation. IL-13Rα2 exists both on the cell membrane, and in soluble form. IL-13Rα2 is relatively rich in hemopoietic or hypervascular tissues, while expressed in low level or not expressed in other tissues. The gene was initially cloned from a kidney cell line and then found to be expressed in brain, spleen, liver, thymus, and also in the bone marrow. The research on IL-13Rα2 has led to the discovery of association of abnormal IL-13Rα2 expression with a number of pathological conditions. The IL-13Rα2 gene polymorphism was found to be involved with susceptibility to Systemic Sclerosis (Brigitte Granel et al. 2006). The overexpression of Il13rα2 gene has been found in brain tumors and ovarian cancer, making IL-13Rα2 one of the candidates as biomarker and target for immunotherapy. In the research by Mitomu Kioi et al in 2006, IL-13 cytotoxin was highly cytotoxic to the IGROV-1 ovarian cancer cell line in vitro, and it mediated significant antitumor activity against a xenografted tumor model. The result suggested that IL-13Rα2 could be a promising target for ovarian cancer therapy. Vaccine therapy of glioma was tested by vaccination using dendritic cells transfected with Il13rα2 mRNA and this experiment induced strong anti-tumor effects in mice (Makoto Saka et al. 2010).