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VEGFs are a family of molecules that are key drivers of vascularization and angiogenic processes. VEGFs induce proliferation and homeostasis of endothelial cells. VEGFs have been studied as indicators of both normal and pathogenic angiogenesis particularly involving tumor cells. Overexpression of VEGF in tumor cells allows tumor growth and enhanced metastatic potential. VEGF family members stimulate cellular responses by binding to VEGF receptors that include fms-like tyrosine kinase (flt-1), KDR gene product (the Mouse homolog of KDR is the flk-1 gene product), and the flt4 gene product. Splicing of the exon 6 or exon 7 mRNA from the 8 exon VEGF gene results in the different amino acid number and variants in humans and mice accounting for VEGF-121, VEGF-165 and others (one amino acid less in Mouse analogs). These variants differ in their binding to heparin sulfate proteoglycans and neuropilin co-receptors imparting differential binding and activation through VEGFRs and variant specific angiogenic or anti-angiogenic functions. VEGFs and VEGFRs are targets for therapeutic intervention.