Several reports indicated AXL as a major driver of resistance to anti-EGFR therapies, e.g., in lung cancer46 and in GBM.47 At the molecular level, AXL-EGFR heterodimerization or transactivation diversify downstream signaling into additional pathways, beyond those triggered by individual receptors, which limits the efficacy of EGFR targeting strategies44,48 and stresses the potential of AXL inhibition in the treatment of EGFR-driven GBM. The gene discussed is EGFR; the disease is glioblastoma.