Migraine has been shown to be associated with increased activity and sensitivity of the trigeminovascular system.[2] This hyperexcitability leads to the activation of nociceptors in the meningeal blood vessels, cerebral arteries, and sinuses, causing headaches and other migraine-related symptoms.[2] Calcitonin gene-related peptide (CGRP) plays a crucial role in migraine pathogenesis.[13] CGRP is expressed in the central and peripheral nervous system and may modulate the trigeminovascular system, leading to pain and other symptoms associated with migraine.[13,14]. This evidence concerns the gene CALCA and migraine disorder.