In standard brain, theLeurocristine side population (SP) phenotype is created by ABC transporter action and identifies stem cell and endothelial cell subpopulations by dye exclusion. By drug efflux, the ABCG2 transporter provides chemoresistance Histone Methyltransferase in stem cells and contributes for the blood brain barrier (BBB) when active in endothelial cells. We investigated the SP phenotype of mouse and human gliomas. In glioma endothelial cells, ABC transporter function is impaired, corresponding to disruption with the BBB in these tumors. By contrast, the SP phenotype is improved in nonendothelial cells that kind neurospheres and therefore are hugely tumorigenic. On this cell population, Akt, but not its downstream target mTOR, regulates ABCG2 activity, and reduction of PTEN increases the SP. This Akt-induced ABCG2 activation effects from its transport for the plasma membrane. Temozolomide, the normal treatment method of gliomas, although not an ABCG2 substrate, increases the SP in glioma cells, specifically in cells missing PTEN.