We demonstrated that endothelial S1PR1-cAbl1 signaling pathway prolonged VEGFR2 signaling augmenting thereby tumor angiogenesis and growth.10 While S1P and VEGF can both independently mediate angiogenesis through activation of their respective receptors, S1PR1 and VEGFR2 in ECs.4 We showed that VEGF alone was weakly angiogenic in S1PR1-depleted ECs corroborating the study shown by LaMontagne et al8 indicating that, that S1PR1 was required for promoting VEGFR2 mediated ECs migration and angiogenesis. This evidence concerns the gene KDR and neoplasm.