They demonstrated that the clearance rate of radiolabeled Aβ in AQP4-deficient mice was reduced by more than 50% compared with wild-type controls, which might result in the formation of extracellular Aβ aggregates and disease progression in AD.1 Further studies using AD murine models have shown that glymphatic transport is markedly suppressed in aged animals, leading to significant Aβ deposition, cerebral amyloid angiopathy, and astrocytic atrophy. The gene discussed is AQP4; the disease is Alzheimer disease.