Experimentally, eNOS-deficient (eNOS−/−) mice display memory deficits and increased levels of APP, β-site APP-cleaving enzyme 1 (BACE1), Aβ, and neuroinflammation in the brain16, indicating a contribution of the loss of eNOS-derived NO to amyloidogenic processing of APP and cognitive decline. The gene discussed is NOS3; the disease is memory.