By combining sophisticated transgenic gain- and loss-of-function strategies with an innovative CRISPR-Cas 9 GBM mouse model in which fluorescently labeled brain tumors are induced from radial glia in the dorsal SVZ, we demonstrate that ASCL1 and OLIG2 are prominent drivers of brain tumor initiation, proliferation, migration, and cell type specification. This evidence concerns the gene ASCL1 and brain neoplasm.