Previously published studies have shown that HDAC 1, 2, and 3 are deregulated during GBM progression31,32 and HDACs negatively regulate estrogen receptors.33,34 Furthermore, the HDAC inhibitor, trichostatin A, sensitizes ERα-negative breast cancer cells to tamoxifen by upregulated expression and nuclear localization of ERβ.35 Our results are in agreement with these published studies and we conclude that HDACi has the potential to reactivate ERβ expression in GBM. This evidence concerns the gene ESR2 and breast carcinoma.