Although VEGF-A infusions in the bloodstream of adult mice can promote V-SVZ neurogenesis, its main receptor, VEGFR2, is expressed by endothelial cells in the V-SVZ, but not by NSPCs, either in physiological conditions or after stroke (Lin et al., 2019); this suggests an indirect effect of systemic VEGF-A on NSPC activity, differently from the proposed direct modulation of V-SVZ neurogenesis by VEGF-C acting through VEGFR3 (Calvo et al., 2011). The gene discussed is VEGFA; the disease is stroke disorder.