CGRP may exert its action in migraine via a range of mechanisms, such as peripheral sensitisation, both through vasodilatation and additional potential indirect effects of CGRP on plasma extravasation, as CGRP stimulates substance P release, which, along with neurokinin A, are the main mediators of plasma extravasation that cause activation of meningeal nociceptors [126]. This evidence concerns the gene TAC1 and migraine disorder.