EGFR and neoplasm: Alteration and/or increased activity in the Wnt, transforming growth factor β (TGF-β), VEGF, epidermal growth factor receptor (EGFR), cyclin-dependent kinase 2A (CDKN2A), nuclear factor-κB (NF-κB), and phosphatidylinositol-3-kinase (PI3K)/AKT/mammalian target of rapamycin (mTOR) pathways may be linked to the GBM pathogenesis and aggressive tumour behaviour [8].