In some gliomas, inhibition of EZH2 may reduce cell proliferation, possibly by de-repressing Ink4a/Arf. However, in other gliomas, loss of EZH2 function could lead to the aberrant expression of factors such as OLIG2, which can drive tumorogenesis (Ligon et al., 2007). Here, CDKN2A is linked to glioma.