The key publication by Akerman et al. [22] demonstrated that AEA decreases trigeminovascular system excitability (primarily involved in a migraine attack) in nitroglycerin (NTG)-induced migraine models; in contrast, the most recent preclinical studies have mainly focused on blocking FAAH and MAGL activities, but a complete dissertation of these publications is beyond the scope of this paper (see [23,24,25] for an overview). The gene discussed is MGLL; the disease is migraine disorder.