Because various combinations of cytokines (i.e., TNF, INFγ, IL-4 and IL-13, and combinations thereof) have been reported to induce IL13Rα2 on a variety of cell types [13]–[15], we reasoned that using similar protocols to increase surface expression of IL13Rα2 on glioma cells would enhance therapeutic efficacy of multiple IL13Rα2-targeting treatment modalities including IL13(E13Y)-zetakine+ CTLs. Here, IL4 is linked to central nervous system cancer.