HK2 loss in vivo resulted in a significant decrease in both tumor vasculature and expression of angiogenic factors such as VEGFA and ANG2, which are key for regulating the hyper-proliferative vasculature in GBMs and triggering the recruitment of bone marrow derived cells in response to radiation, providing a possible escape mechanism for the tumor [31, 45]. The gene discussed is ANGPT2; the disease is neoplasm.