In addition, a recent report showed that overexpression of Sox2, along with other transcriptional factors POU3F2, SALL2, and OLIG2, was sufficient to acquire GSC-like properties.[42] Given the prominent roles of Sox2 in GBM malignancy, it is conceivable that FoxM1-Sox2 signaling axis may be a critical regulator of stem cell maintenance. The gene discussed is FOXM1; the disease is glioblastoma.