Mechanistically, as demonstrated in glioma cells, Src-dependent phosphorylation of CD133 at cytoplasmic residue Y828 promotes its interaction with the PI3K p85 subunit, leading to the translocation of PI3K to the plasma membrane and the initiation of Akt signaling (Fig. 7a), which may promote self-renewal, cell survival and tumorigenicity [163]. This evidence concerns the gene PROM1 and glioma.