Above data suggest that triptolide exerts therapeutic effects on AD by the following mechanisms: 1) inhibiting Aβ deposition by inhibiting BACE1 or CXCR2 in neurons, 2) inhibiting MAPKs activity and attenuating neuroinflammation in microglia, 3) decreasing level of ROS and inhibiting oxidative stress in neurons, 4) attenuating apoptosis and stabilizing mitochondrial membrane potential in neurons, 5) enhancing autophagy in neurons, 6) exerting neurotrophic effects by promoting expression of NGF (in astrocytes), synaptophysin (in neurons), and neuroligin-1. The gene discussed is BACE1; the disease is Alzheimer disease.