In a glioblastoma cell line, the ectopic expression of PTEN, the regulator of PI3K/Akt, disrupted STAT3 signaling and resulted in growth retardation and senescence, whereas the LY294002, another inhibitor of PI3K/Akt, only induced transient dephosphorylation of STAT3 and rapidly restored it to its original level. This evidence concerns the gene AKT1 and glioblastoma.