Correlating the neurological performance of animals 24 h after stroke to the extent of brain tissue damage allowed us to clearly segregate groups by experimental treatment and show that blocking VEGFR2 and potentiating the activation of VEGFR1 by the administration of exogenous ligand, afforded the best level of neuroprotection, closely followed by only blocking VEGFR2 (Figure 3). The gene discussed is FLT1; the disease is stroke disorder.