The targeting glioma cellular pathways, such as the phosphoinositide 3-kinase (PI3K)/protein kinase B (AKT), the p53 pathways, and epidermal growth factor receptor (EGFR) gene amplification or mutation, have failed to show their clinical efficacy due to the high activity of compensatory mechanisms, blood brain barrier selective vulnerability and poor tolerability and safety [57,58]. The gene discussed is AKT1; the disease is glioma.