Noteworthy, in such a contest of bidirectional negative cross-talk between NGB and PPARγ, the expression of such a receptor is lowered during cancer progression in parallel with the increase of NGB in high-grade glioma, strongly sustaining that NGB exerts a critical antiapoptotic function in glioma mainly by protecting cells exposed to accumulating oxidative pressure [54]. This evidence concerns the gene NGB and central nervous system cancer.