VEGF/VEGFR2-activated endothelial cells and potentially other responsive cells in the bone marrow microenvironment can accelerate AML progression, through increased adhesion to AML cells and secretion of cytokines and growth factors that promote leukemic cell growth and viability, including Kitl/SCF, granulocyte-macrophage colony stimulating factor (GMCSF), granulocyte colony-stimulating factor (G-CSF), and IL-6[82,90,91]. This evidence concerns the gene VEGFA and acute myeloid leukemia.