The addition of the isoform HK1 to cells depletedof HK2 does not rescue the aerobic glycolytic phenotype despite a return in totalhexokinase activity, supporting a unique role of HK2 over HK1 in GBM growth.Reduction of HK2 expression in GBM cells has a pronounced impact on invivo anti-tumorgenicity in both subcutaneous and intracranial xenograftmodels (Wolf et al, under review). The gene discussed is HK2; the disease is glioblastoma.