Other data suggest that ciglitazone is able to induce PPAR-γ-independent apoptotic cell death in human T98G glioma cells by down-regulation of Akt and reduction of mitochondrial membrane potential (MMP), an effect that was accompanied by a down-regulation of Bcl-2 expression and an increase in Bid cleavage [76]. This evidence concerns the gene AKT1 and glioma.