This has been confirmed by several groups who have returned to the laboratory to dissect the molecular mechanisms in vitro and animal preclinical models: in GBM cells with low PTEN expression levels, inhibition of the mammalian target of rapamycin, a downstream target of the phosphatidylinositol 3-kinase (PI3K) pathway through Akt (Figure 2), showed substantial efficacy [21–31]. The gene discussed is PTEN; the disease is glioblastoma.