HIF1A and glioblastoma: As mentioned previously, the core regions of GBM are more hypoxic and acidic than the peripheral regions, and hypoxia-inducible factor (HIF)-1α activated by hypoxia via inhibition of HIF-1α prolyl hydroxylation, or by β-catenin/T-cell factor 4 complex binding with STAT3, upregulates the canonical Wnt/β-catenin pathway, which promotes proliferation, invasion, apoptosis, vasculogenesis, and angiogenesis [126].