A microRNA, miR‐27a, has been shown to directly downregulate VE‐cadherin expression.[93] CD5‐2, a target site blocker that specifically blocks miR‐27a/VE‐cadherin interaction, increases expression of VE‐cadherin.[89] Treatment of cerebral cavernous malformation (a disease characterized by a disrupted BBB) model mice with CD5‐2 significantly reduced BBB permeability and the burden of cerebral cavernous malformation lesions.[92]. Here, CD52 is linked to famililal cerebral cavernous malformations.