Finally, a more mechanistic link between an FHM mutation and the induction of a pain phenotype was shown for FHM2 mutant mice; administration of nitroglycerin, used also in migraine patients to elicit migraine-like attacks, resulted in orofacial mechanical hypersensitivity, indicative of migraine-like cranial pain, through changed neuronal activity in the cingulate cortex, a region that is crucial for pain processing [65]. This evidence concerns the gene ATP1A2 and migraine disorder.