In the experimental stroke model, inhibition of CCR2+, which was highly expressed by a subset of monocytes, showed a protective effect on cerebral ischemia damage by producing anti‐inflammatory cytokines, attenuating the infarct volume and brain edema (Bao et al., 2010; Dimitrijevic et al., 2007; Tsukuda et al., 2011). This evidence concerns the gene CCR2 and stroke disorder.