Inhibition of AXL and/or MERTK leads to diminished proliferation, migration and invasion of glioma cells, as well as sensitization of glioma cells to chemotherapy [174–180] Although specific studies addressing the biological role of the TAM RTKs in pediatric HGG and DIPG are not available, overexpression of both AXL and MERTK has been described, and AXL has been shown to be activated in cultured DIPG cells [180, 181]. The gene discussed is AXL; the disease is glioma.