Weldon et al. showed that proliferation followed by activation of microglia and astrocytes were observed around Aβ fibrils and plaques, which precipitated the production of proinflammatory factors, such as tumor necrosis factor-α (TNF-α), interleukin (IL)-1β, and IL-18, in the AD brain models [134]. The gene discussed is IL1B; the disease is Alzheimer disease.