Recent studies that have attempted to decode the molecular mechanisms involved in hypoxic cell adaptation in glioblastoma have shown that the major signalling pathways activated in hypoxia are those of the hypoxic inducible factor 1α (HIF-1α) vascular endothelial growth factor (VEGF), transforming growth factor beta (TGFβ), mammalian target of rapamycin (mTOR), CD133, as well as of signal transducer and activator of transcription 3 (Stat3) [6–9]. Here, HIF1A is linked to glioblastoma.