While the latency of gliomas induced in Ntv-a Ink4a/Arf+/-Pten+/fl mice by RCAS-PSG and RCAS-Cre was intermediate between the wild type and Ink4a/Arf-/-Ptenfl/fl mice, the distribution of glioma grades at the point when the tumors caused mice to become moribund was similar to that of gliomas characterized by homozygous tumor suppressor loss at initiation (Figure 2a; Figure S4b). Here, CDKN2A is linked to glioma.