Otx2 has been shown to promote cell cycle progression and inhibit differentiation in medulloblastoma cells [13], thus it is possible that cell cycle deregulation by Otx2 underlies both tumor maintenance in established medulloblastomas [9], [13] and mitogenic niche-independent proliferation of neuronal progenitor cells in GFAP:Hi-Otx2 mice. Here, GFAP is linked to neoplasm.