EMX2 and glioblastoma: Interestingly, the magnitude of EMX2 upregulation upon EZH2i treatment varied from a 2‐fold to 250‐fold change in the different GBM cell lines, and inversely correlated with the degree of DNA methylation at the EMX2 promoter, again suggesting that DNA methylation could act as a redundant mechanism to repress PRC2 targets (Fig 3H).