AKT1 and glioblastoma: The mechanism of action of 17-AAG is similar to its parent compound, i.e., it acts through blockade of HSP90 activity with consequent direct degradation of its client proteins, such as Akt/MAPK/Rb, and abolition of downstream target phosphorylation (e.g., MEK, Cdk4 and 6), independent of GBM mutations in TP53, PTEN, or EGFR.