Although it is tempting to speculate that RhoG activity may compensate for Rac1 in wild-type endothelial cells, thus explaining the reduced requirement for Rac1 in wild-type angiogenic events in vivo, this is also not likely because Rac1-deletion in both β3-null and wildtypes brings tumor growth and blood vessel density to the same level in both genotypes. The gene discussed is RHOG; the disease is neoplasm.