Because human high-grade glioma has additional deletions and mutations, such as loss of CDKN2A, which results in the disruption of cell cycle arrest pathways [25, 26], we further determined whether loss of CDKN2A is required for kRas- and Akt3-induced glioma by injecting CDKN2A-null Ntv-a transgenic mice with RCAS-kRas and RCAS-Akt3. The gene discussed is KRAS; the disease is central nervous system cancer.