Robust experimental evidence indicates that elevated CCL2 levels induce the recruitment of macrophages, production of cytokines, and direct alteration of the expression of endothelial cell tight-junction proteins to increase blood–brain barrier (BBB) permeability, observed during various pathological processes, such as multiple sclerosis [33, 34], stroke [35, 36], and Alzheimer’s disease [37, 38]. This evidence concerns the gene CCL2 and Stroke.