The example in point is the antitumor agent PI-88 (muparfostat), which retards tumor growth via inhibiting angiogenesis in two ways: 1) interaction with pro-angiogenic growth factors such as vascular endothelial growth factor (VEGF) and fibroblast growth factor (FGF) and 2) by prevention of the release of angiogenic growth factors from the extracellular matrix (ECM) via inhibition of heparanase [19–22]. The gene discussed is VEGFA; the disease is neoplasm.