Similarly, in AD, over-activated microglia contribute to heightened production of inflammatory cytokines, triggering a positive feedback loop; genetic polymorphisms of several cytokines, such as interleukin (IL)-1α, IL-1β, IL-6, and tumor necrosis factor (TNF), modify the risk of AD development and progression in certain populations (Su et al., 2016). Here, IL1B is linked to Alzheimer disease.