Acute brain damage after ischemia is usually related to the activation of microglia, which are major cell to post-injury inflammation [24], and M1 (classical activation phenotype) microglia will lead to brain damage through producing pro-inflammatory and neurotoxic cytokines, such as TNF-α and IL-1β, their levels peaking at 24 or 48 h after stroke [25,26]. Here, IL1B is linked to ischemia.