Importantly, potent additive or synergistic activity of the trametinib + FAK inhibitor combination is observed across multiple murine and human models and is independent of BRAFV600E mutation status or specific compensatory signaling mechanisms, suggesting that this combination may serve a wider population of GBM patients than current personalized treatment propositions, such as the trametinib and dabrafenib combination, which is currently restricted to 1–2% of GBM patients that express the BRAFV600E mutation [13,14]. Here, PTK2 is linked to glioblastoma.