Before GFAP mutations were discovered to cause AxD, a common pathogenesis with AD was suggested based on the oxidative injury response, including advanced glycation end products and lipid peroxidation adducts associated with both Rosenthal fibers, the hallmark GFAP aggregates in AxD, and neurofibrillary tangles in AD [59]. The gene discussed is GFAP; the disease is Alzheimer disease.