ChIP-Seq coupled with systemic metabolite profiling in GBM models revealed that the suppression of c-Myc, a pro-survival factor and a major regulator of glycolysis, can be achieved with HDAC inhibitors (panobinostat, vorinostat, and romidepsin), which have been discovered to reduce glycolysis in GBM by reducing c-Myc protein levels and improve survival rates in GBM-bearing animals [113,114]. The gene discussed is HDAC9; the disease is glioblastoma.