Cumulative experimental evidence showed that p38 and JNK MAPKs could be activated in neurons, microglia, and astrocytes after various types of ischemia [66–69], and their activation was associated with the production of proinflammatory cytokines, such as TNF-α and IL-1β, which tend to act as perpetrators in the CNS injury [70, 71]. Here, IL1B is linked to ischemia.