DMF treatments have been found to ameliorate cognitive deficits, mitigate tauo-/amyloidopathy, and inhibit microglial oxidative/inflammatory responses presumably through modulating the activities of AMPK/SIRT-1, AKT/CREB/BDNF, AKT/GSK-3β, adiponectin/Adipo1R, and NF-κB/IL-1β/ROS trajectories in AD mouse models [127]. The gene discussed is AKT1; the disease is Alzheimer disease.