EGFR and glioblastoma: 29). GBM cells can exploit the ECM to facilitate migration, and they can secrete proteolytic enzymes, such as matrix metalloproteinases (MMPs), which degrade ECM components and create paths for cell migration (Refs. 11, 35, 39–41). They can also switch from a mesenchymal-like to amoeboid-like way of cell migration when challenged with specific inhibitors. Moreover, several compounds were targeting VEGF and epidermal growth factor receptor (EGFR), as well as various signaling pathways to inhibit GBM cell migration (Refs. 35, 42–44).