Hu et al. found that microglia responded dynamically to I/R brain injury and experienced a transition to a ‘sick’ M1 phenotype similar to macrophages in the early phase of cerebral ischemia.[16,17] This microglial phenotype was identified as a proinflammatory and neurotoxic phenotype and expressed high levels of CD86, CD11b and iNOS. This evidence concerns the gene CD86 and Cerebral ischemia.