Both TPI1 and PKM2 promote histone acetylation through nuclear translocation, especially nuclear translocation of TPI1, which leads to significant histone acetylation in several types of cancer cells by modulating histone deacetylase (HDAC) activity.[7, 10] Therefore, we performed HDAC activity assays and WB to determine whether changes in histone acetylation occurred in TMZ‐resistant GBM cells and Linc00492‐overexpressing GBM cells. This evidence concerns the gene TPI1 and glioblastoma.