HIF1A and glioblastoma: In contrast, transcriptional activation of a PDK1 minigene by other transcription factors fails to modulate PDK1 RNA splicing without endogenous HIF1α target gene activation.44 HIF1α stabilization stimulated glycolysis in bone by upregulating crucial glycolytic enzymes including PDK1.45 In glioblastoma multiforme, the inhibition of HIF1α with chrysin reduced the expression of PDK1, PDK3, and GLUT1 and significantly promoted cell death under both normoxic and hypoxic conditions.46 Additionally, some studies described that SIRT3 reduces the production of ROS in some other cancers.