For instance, β-catenin signaling was linked to the generation of CD133+ glioma stem cells [25] as well as linked to the increased oncogenic activity of EGFR [26]; more importantly, CDK6 has been shown to be an emerging target for drug development for GBM where CDK6 expression/activity is elevated in GBM cells and inhibitor of CDK6 could significantly suppressed GBM in vitro and in vivo [27]. This evidence concerns the gene PROM1 and glioblastoma.