Morosetti et al. reported that human glioblastoma cell lines, such as A172 and U87-MG, also express high levels of PPARγ, which rosiglitazone inhibited proliferation of those cell lines by G2/M arrest and apoptosis, and that the growth inhibitory effect was partially reversed by the PPARγ antagonist GW9662 [9], suggesting that it may work through PPARγ-dependent and PPARγ-independent pathways. Here, PPARG is linked to glioblastoma.