This mechanistic paradigm and proposed sequence of molecular events (Fig 4) is attractive because it integrates ApoE and ApoJ genetics and biology with many previously disjointed observations such as extensive lipid peroxidation in AD brain, and environmental triggers for lipid peroxidation that are known or suspected AD risk factors (reviewed in [15]), into one unifying explanation for human sporadic AD. The gene discussed is CLU; the disease is Alzheimer disease.