“Angiogenesis switch” in leukemia is documented by increased bone marrow MVD (Figures 2(a) and 2(b)), increased expression of HIF-1, multiple proangiogenic factors (VEGF, bFGF, angiopoietin-2), soluble VEGFR, and decreased expression of endogenous angiogenesis inhibitors, such as thrombospondin-1 [11, 12]. The gene discussed is FGF2; the disease is leukemia.