A widel-accepted mechanism posits that migraine pain is caused by activation of the trigeminovascular system (Noseda and Burstein, 2013; Akerman et al., 2017; Ashina et al., 2019), which involves algogenic and inflammatory substances such as nitric oxide, calcitonin gene-related peptide (CGRP), neurokinin A, substance P, prostaglandins, and cytokines in the meninges, whereby their release would influence the activation of trigeminovascular afferents (Goadsby and Edvinsson, 1993; Gallai et al., 1995; Sarchielli et al., 2000, 2006). This evidence concerns the gene TAC1 and migraine disorder.