TCF4 and glioblastoma: Accordingly, we demonstrated that the Wnt signaling-induced formation of a HIF-1α/TCF1/β-catenin complex activates a potent pro-neuronal transcriptional program in GBM cells, which is counteracted, in normoxia, by the accumulation of high-molecular-weight TCF4 isoforms, which act as transcriptional repressors and prevent the complex binding to DNA [125] (Figure 3).