This may be as a result of mutations in its receptor tyrosine kinases (EGFR-45%, Erb-B2 receptor tyrosine kinase 2 (ERBB2)-8%, platelet-derived growth factor receptor alpha (PDGFRA)-13%, and MET-4%), core oncogenes (RAS-2%, PI3K-15%, and AKT-2%), or tumor suppressors (phosphatase and TENsin homolog (PTEN)-36%, neurofibromatosis type 1 (NF1)-18%, and forkhead box O (FOXO)-1%) in patients with GBM (7). Here, AKT1 is linked to glioblastoma.