In particular, the finding of an association between SOD2 Ala16Val polymorphism and the occurrence of unilateral cranial autonomic symptoms (UAs) during the attack in MWA lead to the hypothesis that SOD2 polymorphism may cause a defective control of the oxidative phenomena linked to cortical spreading depression (CSD), the neurophysiological hallmark of migraine aura, causing an overstimulation of trigeminal neurons and UAs triggering [25]. The gene discussed is SOD2; the disease is migraine disorder.