(i)lead to the caspase-dependent cell apoptosis and an accumulation of cells in phase G0/G1 in a dose-dependent fashion, thus, resulting in the reduction of cell activity and the promotion of LDH release, (ii)attenuate cell invasion and migration of GBM, (iii)induce the death of GBM cells through suppressing mGluR1/PI3K/AKT/mTOR signaling,(iv)inhibit GSC cell growth through inhibition of glucose transporter 3 (GLUT3) that associates with a decrease in p-AKT/HIF1 alpha pathway. This evidence concerns the gene AKT1 and glioblastoma.