Aberrant histone modifications are implicated in the development and progression of GBM.29 Specifically, HDACs, which cause histone deacetylation, and histone methyltransferases and demethylases that promote alteration in histone methylation are implicated GBM progression.30 Our results demonstrated that HDACi but not inhibitors of methyl transferases enhance expression of ERβ and suggest that alternations in histone acetylation may contribute to suppression of ERβ expression during GBM progression. This evidence concerns the gene ESR2 and glioblastoma.