Our finding is consistent with a recent paper that reported FoxM1-mediated Sox2 induction in neuroblastoma cells.[37] Importantly, our data that FoxM1 overexpression upregulated Sox2 expression in GBM cells, and that ectopic expression of Sox2 rescued FoxM1 inhibition-mediated effects further support that Sox2 is a key downstream regulator of FoxM1 signaling in GBM. The gene discussed is FOXM1; the disease is neuroblastoma.