FLIP levels in TRAIL-resistant cells are regulated by the phosphatase and tensin homologue (PTEN)-AKT-mammalian target of rapamycin (mTOR) pathway, and PTEN loss and AKT activation are correlated with increased FLIPS mRNA translation, high levels of FLIPS expression, and TRAIL resistance in vitro, in human glioblastoma multiforme (GBM) xenografts and in primary human GBM samples [11]. The gene discussed is PTEN; the disease is glioblastoma.