These changes are reminiscent of glioma pathogenesis and include decreased or absent expression of the tumor suppressors Pten, Ink4a and Arf, and overexpression of Egfr, the p53 antagonist Mdm2, and the cell cycle regulator, Cdk4. Such findings perhaps bolster the physiologic relevance of this mouse model despite its reliance on a mutated Ras protein not characteristic of glioma biology. This evidence concerns the gene CDKN2A and central nervous system cancer.