We have previously reported that miR‐15a/16‐1 can negatively regulate the expression of Bcl‐2, claudin 5, VEGFA, FGF2, VEGFR2, and FGFR1 to modulate post‐stroke cerebrovascular injury and remodeling.[15, 16] We have shown that genetic deletion or pharmacological inhibition of miR‐15a/16‐1 activity provides brain protection and repair in experimental stroke by inhibiting apoptosis, maintaining blood‐brain barrier integrity, and promoting cerebral angiogenesis. Here, CLDN5 is linked to Stroke.