In fact, while microglia phagocytic capacity contributes to CNS neuroprotection from excessive Aβ, microglial activation by Aβ soluble oligomers promotes excitotoxicity and neurodegeneration by the release of several inflammatory cytokines, such as tumor necrosis factor (TNF)-α and interleukin (IL)-1β, contributing to the onset and progression of AD [26,27]. The gene discussed is TNF; the disease is Alzheimer disease.