In many tumor cells, including glioma cells, NO can activate pro-survival signaling pathways by modifying effector proteins such as soluble guanyl cyclase (sGC), hypoxia-inducible fctor-1α (HIF-1α), extracellular signal-regulated kinases-1 and −2 (ERK-1/2), epidermal growth factor receptor (EGFR), or protein kinase-B (Akt) via phosphoinositide-3-kinase (PI3K)[22–25]. This evidence concerns the gene AKT1 and glioma.