HIF1A and glioblastoma: Notably, we show that TYRO3 and EPHA7, in addition to PDGFRA and ERBB3 (known HIF1α targets [43, 44]), are direct transcriptional targets of HIF1α in GSC, which can potentially account for the enigmatic RTK co-activation that occurs in GBM [45] (Supplementary Fig. 5A).