In contrast, HDAC I overexpression has been reported in high-grade, late-stage proliferative tumors, supporting the rationale for the use of HDAC inhibitors in promoting the re-expression of silenced tumor suppressor genes in glioblastoma, as well as a more open chromatin structure facilitating access for DNA damaging agents (66, 67). Here, HDAC9 is linked to glioblastoma.