The expression of two angiogenic agents, vascular endothelial growth factor-A (VEGF-A) and the angiopoietin-2 (Ang-2) on AML cells is associated with poorer patient outcome.74, 75 Circulating levels of Ang-2 and VEGF are also strong predictors of poor survival in AML patients.76, 77, 78 The expression of VEGF-A and its receptors on AML cells is increased, raising the possibility of an autocrine proliferation mechanism in AML.79 Bispecific antibodies have been generated to simultaneously target VEGF-A and Ang-2. The gene discussed is VEGFA; the disease is acute myeloid leukemia.