It plays a pivotal role in the cooption of host vessels in the initial phase; and in supporting in-situ tumor angiogenesis, while in the second phase it allows destabilization of mature vessels, by antagonizing Ang1-mediated Tie2/TEK activation, in order to facilitate mitogenic stimulation of ECs by VEGF and promoting tumor neovascularization [22, 24]. This evidence concerns the gene TEK and neoplasm.