SOD1 has not been reported in AAA, but when treated with hydroxyl ethanol, it inhibits Ang II-induced Alzheimer’s disease, decreases the expressing of NF-κB, P65, TNF-α, and IL-1β, and increases the conveying of SOD1, MMP9, and GCLC in mice [34]. The gene discussed is GCLC; the disease is triple-A syndrome.