Increased levels of pro-inflammatory cytokines, such as tumor necrosis factor (TNF)-α, interleukin (IL)-6 and IL-1β, are believed to inhibit phagocytosis of Aβ and promote phosphorylation and cleavage of APP, thereby exacerbating accumulation of Aβ in AD brains31–35. The gene discussed is TNF; the disease is Alzheimer disease.