[9] improved the resistance of GBM toTMZ by inhibiting mTOR with rapamycin and reducing the expression of SOX2, reversing thepoor prognosis of GBM. Oppel et al. [75] reported that SOX2 can regulate the migration and invasion of GBM cellsthrough the RhoA-dependent pathway and focal adhesion kinase (FAK) signaling. Furthermore,SOX2 is involved in four major signaling pathways—TGF-β, SHH, EGFR, and FGFR, and isregulated by these pathways, affecting the progression of GBM [76]. The gene discussed is PTK2; the disease is glioblastoma.