This indicated that NO is involved in the pain mechanism in both types of migraines but not in the initiation of the aura.[24] Further study demonstrated that not NO itself but the elevation of cGMP by NO or other mediators is necessary to induce migraine.[26] Inhibition of NOS in spontaneous migraine attacks leads to the attenuation of symptoms in two-thirds of the patients.[27] Thus, NO seems not only be involved in the initiation of migraine attacks but also in the maintenance of these attacks. Here, NOS2 is linked to migraine disorder.