VASH1 was originally identified as an endothelium-derived vascular endothelial growth factor (VEGF)-inducible angiogenesis inhibitor that acts in a negative feedback manner. VASH1 mRNA is expressed brain, heart, kidney and placenta in the adult, with robust expression in various organs during embryonic development. VASH1 expression in tumor cells and tumor vasculature is silenced by methylation by increased expression of Zeste homolog 2 (EZH2). The increase of EZH2 expression is induced by VEGF stimulation, leading to poor clinical prognosis. Recombinant adenovirus expressing VASH prevented tumor angiogenesis and inhibited tumor growth, suggesting that it may be a potentially valuable antitumor therapy in the clinic.