In models of Alzheimer disease produced by overexpression of APP/PS1 or human APP, CX3CR1 knockout results in decreased levels of pro-inflammatory cytokines Tumor Necrosis Factor (TNF) and monocyte chemotactic protein 1 (CCL2) but increased Interleukin 1-beta (IL1β) [29,33,34]. The gene discussed is TNF; the disease is early-onset autosomal dominant Alzheimer disease.