In GBM mouse model systems, scientists found that tumor aggression increased and the infiltration of a large number of immune cells, such as TAMs and other CD11b+ myeloid cells emerged in the brain after treating recurrent GBM patients with bevacizumab or the angiokinase inhibitor cediranib, despite the immune privilege in the normal human brain (119, 193–195). The gene discussed is ITGAM; the disease is glioblastoma.