These phenomena illustrate three problems: first, the SOX2-AKT/STAT3-Slug signaling pathway could mediate the therapeutic effect of NF in GBM; second, the SOX2-AKT/STAT3-Slug signaling pathway was the dominant target of NF; and third, NF also had other targets independent of the SOX2-AKT/STAT3-Slug signaling pathway. Here, AKT1 is linked to glioblastoma.