AKT1 and glioblastoma: In GBM, the PI3K/AKT pathway is often constitutively activated due to various genetic and epigenetic alterations, such as mutations in PI3KCA, PTEN and AKT1/2/3 genes, as well as loss of PTEN expression and activation of oncogenic receptor tyrosine kinases (RTKs) such as PDGFRA and IDH1R132H17-19.