Previous studies show that plagues, tangles, and neuronal debris persistently activate primed microglia, which results in a constant production of proinflammatory mediators, such as interleukin-1 beta (IL-1β), tumor necrosis factor alpha (TNF-α), nitric oxide, chemokines, and complements [5, 6] These mediators maintain microglial activation and induce neuroinflammatory responses in early phase of AD, which aggravate tau pathology, synaptic, and neuronal dysfunction. The gene discussed is IL1B; the disease is Alzheimer disease.