In 3xTg-AD mice, Bcl2 and Bax levels were not significantly different between nonTg+GFP and 3xTg+GFP, but treatment with AAV-NF-α1/CPE-E342Q or AAV-NF-α1/CPE increased Bcl2 (Fig 3G) and decreased Bax (Fig 3H), indicating the effect of NF-α1/CPE on enhancing the Bcl2-mediated pro-survival cascade. The gene discussed is BCL2; the disease is Alzheimer disease.