Prior studies have implicated TrkB in the survival of brain tumor initiating cells in the absence of growth factors epidermal growth factor (EGF) and fibroblast growth factor (FGF)11, while more recent work has implicated TrkB and its ligand, brain-derived neurotrophic factor (BDNF), in the crosstalk between glioma stem cells and their differentiated glioblastoma cell progeny12, suggesting that this neurotrophin receptor exhibits complex interactions within the brain tumor environment that extend beyond the canonical TrkB-BDNF signaling events characterized in normal neurodevelopment. The gene discussed is EGF; the disease is glioma.