In addition, αPK treatment significantly increased claudin-5, occludin, and ZO-1 co-localization with vessels in the peri-infarct area, while the infarct core was unaffected at day 7 after stroke compared to control mice (Fig. 3F–H), suggesting stabilization of the BBB by PK blockade in the subacute stroke phase. The gene discussed is CLDN5; the disease is Stroke.