Given the fact that 10 μM doses of troglitazone allay TGF-βrelease of glioma cells (F98, SMA-560, U-87 MG) by more than 50% [9], we hypothesized that the abrogation of gliomacell motility and invasiveness by troglitazone and other PPARγactivators is primarilydriven by the inhibition of TGF-β signaling and thus, troglitazone and relatedcompounds may be considered for adjuvant glioma therapy to counteract TGF-β-mediatedbrain invasion. Here, TGFB1 is linked to central nervous system cancer.