AKT1 and glioblastoma: This overexpression is associated with increased proliferation and migration of glioblastoma cells (U-87MG and U-118MG), recurrence, poor overall survival, alterations in the signaling pathways involved in tumor progression and aggressiveness (e.g., JAK-STAT, NF-κB, Akt), and somatostatin analog resistance, since the silencing of this somatostatin receptor variant sensitizes glioblastoma cells to the antitumor action exerted by the somatostatin analog pasireotide [103].