Notably, the PI3-kinase/Akt pathway is frequently hyperactivated in GBM, supporting the maintenance and self-renewal of GSCs, contributing to tumor initiation and resistance to therapy.35 Further, previous studies, including our own, have further demonstrated that the PI3-kinase/Akt signaling pathway regulates the stemness and dormancy properties of GBM cells.27,36 Notably, the PI3-kinase (and Akt) activity is also known to be modulated by ROS.37 This evidence concerns the gene AKT1 and glioblastoma.