In order to definitively support the already described pro-oncogenic function of TCF4 [9] and further sustain its involvement in the HDI-mediated reduction of the GBM stem cell phenotype, we treated GBM cells, transiently over-expressing a Myc-tagged TCF4, with both TSA and SAHA, as described, and demonstrated that increased levels of hMW TCF4 are sufficient to partially, although significantly, counteract the previously reported dramatic reduction of CD133 levels upon HDI exposure (Figure 1F,G and Supplementary Figure S1D,E). Here, TCF4 is linked to glioblastoma.