However, we report that active levels of Rac1 are increased in β3-null endothelial cells and that the enhanced tumor growth, tumor angiogenesis and VEGF-mediated responses in β3-null mice were all dependent on endothelial Rac1 expression since Rac1-depletion in β3-null endothelial cells reduced significantly these responses. The gene discussed is VEGFA; the disease is neoplasm.