In summary, we report that ischemic stroke in C57BL/6J mice triggers time-dependent changes in the blood-CSF barrier permeability, tight-junction damage and dynamic changes of SPAK-NKCC1 complex pathway at 1–7 days post-stroke, reflected by an elevation of albumin permeability, transient increase of SPAK-NKCC1 protein phosphorylation, elevation of proinflammatory Lcn2 mRNA and protein expression, and immune cell infiltration into the ChP (Figure 8). The gene discussed is STK39; the disease is Stroke.