Using AAV-hTau injected into the hippocampus of 2-m-old C57 mice to mimic intraneuronal tau accumulation as seen in the majority of AD cases, we found that overexpression of hTau acetylated STAT1 to increase STAT1 binding with STAT3 in the cytoplasmic fraction, and then, decreased STAT3 translocation into the nucleus and inactivated STAT3, though phosphorylated level of STAT3 at Tyr705 increased. The gene discussed is MAPT; the disease is Alzheimer disease.