Activation of the trigeminovascular pain pathways is thought to mediate part of the qualities of migraine pain by release of neuropeptides, such as calcitonin gene-related peptide (CGRP) and pituitary adenylate cyclase activating polypeptide (PACAP), at the level of the dura mater [13–15]. This evidence concerns the gene ADCYAP1 and migraine disorder.