Tumor hypoxia represents a potent stimulus for continued induction of several key angiogenic cytokines, including the vascular endothelial growth factor (VEGF) [9, 10] and its endothelial-specific receptors VEGFR1 (Flt1) and VEGFR2 (KDR/Flk1) [11, 12]. This evidence concerns the gene FLT1 and neoplasm.