Loss of cell-cell contact with healthy neurons [102–104] and receptor activation in response to extracellular glutamate accumulation [105] during ischemic stroke polarize microglia toward the pro-inflammatory M1 phenotype, which secretes factors such as tumor necrosis factor-alpha (TNF-α), interleukin-1 beta (IL-1β), and reactive oxygen species [106]. Here, IL1B is linked to ischemic stroke.