The mechanisms may be related to the inhibition of the β-secretase processing of APP and Aβ production, accompanied by the amelioration of tau hyperphosphorylation by restoring the glycogen synthase kinase-3β (Gsk3β) phosphorylation at the Ser9 site in the hippocampus of 3 × Tg-AD mice. The gene discussed is GSK3B; the disease is Alzheimer disease.