This further contributes to the modulation of the local perivascular microenvironment generating a supporting milieu, designated as the pre-metastatic niche.14–17 Moreover, there is evidence that increased expression of Ang-2 in endothelial cells of co-opted blood vessels facilitates vascular destabilization and regression, leading to hypoxia-induced upregulation of Ang-2, VEGF, and subsequent induction of angiogenesis at the tumor margin.12 Several preclinical studies have demonstrated that therapeutic targeting of Ang-2 and/or VEGF can slow tumor growth and reduce tumor angiogenesis. The gene discussed is ANGPT2; the disease is neoplasm.