Early observations of neuritic plaques composed of amyloid β and neurofibrillary tangle-laden neurons surrounded by reactive astrocytes and microglia [1–4], as well as evidence that microglia exposed to amyloid β release proinflammatory factors such as interleukin 1 beta (IL-1β) and tumor necrosis factor alpha (TNFα) [5–7] that in turn could modify AD pathology [8–12], led to hypotheses positing chronic neuroinflammation as a driving feature of AD [13]. The gene discussed is IL1B; the disease is Alzheimer disease.