This causes the activation of VEGFR2 and the trafficking of the α4β1-VEGFR2 complex to the leading edge of the cell where it facilitates tumor, or endothelial cell, migration via Rac1 (Ras-related C3 botulinum toxin substrate 1) activation and the reorganization of the actin cytoskeleton (45). This evidence concerns the gene RAC1 and neoplasm.