It has been shown that NLRP3 inflammasome was activated in the TNC (a central region related to migraine pain) and apoptotic marker (CC3) was increased in the trigeminal ganglia (a peripheral region related to migraine pain) in an NTG-induced migraine mouse model, suggesting that NLRP3 inflammasome activation and apoptosis may be at least partially responsible for migraine pain sensitization (including peripheral and central sensitization) [33, 46]. This evidence concerns the gene NLRP3 and migraine disorder.