For example, FoxM1 is not only required for pluripotency maintenance of P19 embryonal carcinoma cells by regulating Oct4,43 but also enhances tumorigenesis of glioblastoma cells by promoting the nuclear translocation of β-catenin, a critical mediator of Wnt signaling, via a direct protein-protein interaction.55 Taken together, these findings support our data that the cytotoxic effect of thiostrepton on CRSCs is due to higher expression of FoxM1 in these cells and explain the decreases in both SC subpopulations and the susceptibility to this antibiotic observed in FoxM1-knockdown clones. The gene discussed is POU5F1; the disease is glioblastoma.