Several vascular risk factors may limit this endogenous vessel capacity in the adult brain, especially during aging when there are collateral rarefaction and deficient recruitment [22]s Since NBP was shown to enrich vascular factors bFGF, HIF-1α, and VEGF to increase angiogenesis and reduce neurovascular inflammation after stroke [23-25], we hypothesized that NBP could promote post-stroke arteriogenesis including collateral arteries as a underlying mechanism for its protective and regenerative effects. The gene discussed is VEGFA; the disease is Stroke.