In this process, nuclear factor-κB (NF-κB) and its pathways can be activated by oxidative stress [16], cerebral ischemia, and hypoxia, triggering a myriad of pro-inflammatory responses in microglia after brain ischemia, including upregulation of inflammasome components, such as tumor necrosis factor-alpha (TNF)-α, interleukin (IL)-6, IL-1β, which can further increase inflammatory damage [17]. The gene discussed is IL1B; the disease is brain ischemia.