Endothelium-targeted deletion of miR-15a/16-1 not only promoted post-stroke angiogenesis by enhancing the expression of vascular endothelial growth factor A (VEGFA), fibroblast growth factor 2 (FGF2), vascular endothelial growth factor receptor 2 (VEGFR2), and fibroblast growth factor receptor 1 (FGFR1), but also ameliorates post-ischemic blood-brain barrier dysfunction via up-regulating claudin-5 expression (Yang et al., 2017). This evidence concerns the gene FGFR1 and Stroke.