Excessive activated microglia at the onset of ischemia sense the microenvironmental changes through diverse receptors including Toll-like receptors (TLR), Nod-like receptors and C-type lection receptors, thereafter enhancing the release of neurotoxic matters, such as superoxide, matrix metalloproteinases and several cytokines [e.g., interleukin-1β (IL-1β), interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-α)], which induces astrocyte activation, determines the fate of astrocyte (Jha et al., 2019) and aggravates ischemic brain injury. The gene discussed is IL1B; the disease is ischemia.