PTK2 and glioblastoma: Indeed, FAK and other RTKs, including epidermal growth factor receptor (EGFR), platelet-derived growth factor receptor (PDGFR), and vascular endothelial growth factor receptor (VEGFR), determine the loss of SRC interdomains interactions involved in SRC inhibition, leading to most of the GBM-associated phenomena [9,18,19,20].