The mechanisms by which onabotulinum toxin A ameliorates migraine include increasing the threshold for nociceptive activation by decreasing circulating levels of neuropeptides such as CGRP, decreasing the number of TRPV1‐immunoreactive neurons in the trigeminal ganglia, decreasing dorsal horn neuron activation, and decreasing the expression of nitric oxide synthase in the central nervous system.7 This evidence concerns the gene TRPV1 and migraine disorder.