As reported, intravenous (i.v.)administration of FGL-NP(Cit)/HNSS in 3xTg-AD mice has reversed mitochondrial dysfunction via the PGC-1α and STAT3 pathways, inhibited Aβ deposition and tau hyperphosphorylation, and ameliorated memory deficits and cholinergic neuronal damage [36]. The gene discussed is STAT3; the disease is Alzheimer disease.