The level change of IFN-γ in AD patients has not been reported, however, overexpressing IFN-γ results in a significant decrease of Aβ deposits and infiltration of peripheral monocytes [63], which is consistent to the observations that IFN-γ increases Aβ uptake by microglia and activates microglia to facilitate T cell motility and synapse formation in vitro [64]. The gene discussed is IFNG; the disease is Alzheimer disease.