Therefore, we aim to define how H<sub>2</sub>O<sub>2</sub> signaling regulates SH3GLB1 and AKT (protein kinase B) pathways in GBM and to assess whether modulating H<sub>2</sub>O<sub>2</sub> reverses temozolomide (TMZ) resistance.<h4>Methods</h4>We used cultured cells and pharmacological inhibitors and activators to confirm the significance of H<sub>2</sub>O<sub>2</sub> signaling. This evidence concerns the gene AKT1 and glioblastoma.