The transactivation of β-catenin enables EGFR activation, leading to GSC expansion, metastasis, differentiation, tumor formation (149), and subsequently the human oncogenic EGFR is over-expressed, enhancing the self-renewal ability of GSCs, and further contributing to tumor- initiation or tumor- proliferation in GBM (36, 63, 64). This evidence concerns the gene EGFR and glioblastoma.