Moreover, the levels of miR-124, which directly induced a posttranscriptional deregulation of Fpn, also increased in AD patients; (2) Iron accumulation aggravated toxic Aβ deposition and tau hyperphosphorylation, which disrupted GSH synthesis and reduced Gpx4 levels (3); (4) Elevated LOX catalyzed PUFAs and generated ROS via Fenton reaction. The gene discussed is LOX; the disease is Alzheimer disease.