First, the double-inactivation of endothelial Epn1 and Epn2 resulted in elevated and prolonged VEGFR2 phosphorylation as well as in the stabilization of VEGFR2 protein, leading to heightened VEGF/VEGFR2 signaling and excessive tumor angiogenesis in mice 17, 46. Here, EPN1 is linked to neoplasm.