Consequently, TNF-α genetic deletion reduces plaque formation by lowering Aβ generation in AD mice [19], and genetic ablation of TNF-α receptor-1 or administration of TNF-α modulator/inhibitors to AD mice results in attenuation of the Aβ pathology [18, 20–23], suggesting that inhibition of TNF-α signaling confers a protective effect against AD pathology. The gene discussed is TNF; the disease is Alzheimer disease.