Given the fact that the soluble and the membrane bound VEGFR-1 potently sequester VEGF binding to the vascular endothelial growth factor receptor 2 (VEGFR-2), VEGF/VEGR-2 signaling[21], a major driving force for tumor angiogenesis, is inhibited upon COUP-TFII depletion. This evidence concerns the gene NR2F2 and neoplasm.