In response to any type of pathologic events (injury, infection, and inflammation) or changes in brain homeostasis, microglia rapidly switch to an activated state, undergo substantial morphological, molecular, and functional changes, and produce a broad spectrum of proinflammatory mediators, such as nitric oxide (NO), reactive oxygen species (ROS), and proinflammatory cytokines, including interleukin 1beta (IL-1β), IL-6, and tumor necrosis factor-alpha (TNF-α), resulting in inflammation-induced neuronal cell damage or death [3]. The gene discussed is TNF; the disease is infection.