Activation of VEGFR2 results in the activation of phosphatidylinositol 3-kinase (PI3K) which plays an important role in regulating endothelial proliferation, migration and survival (Jiang et al. 2000). Activation of PI3K is also essential for VEGF-stimulated nitric oxide (NO) production from endothelial cells via protein kinase B (PKB/AKT) signaling to eNOS (Nitric oxide synthase, endothelial) (Blanes et al. 2007). Upon stimulation by VEGF the p85 regulatory subunit of PI3K is recruited to phosphorylated tyrosine-801 of VEGFR2 (Dayanir et al. 2001).