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. The gene discussed is TP53; the disease is central nervous system cancer.