This hypothesis states that the pain in migraine originates from the trigeminovascular system—activation of the trigeminal sensory nerves releases several vasoactive neuropeptides, including calcitonin gene-related peptide (CGRP), neurokinin A, and substance P. Release of these vasoactive neuropeptides triggers cerebral vasodilation and dural plasma extravasation, leading to neurogenic inflammation. The gene discussed is TAC1; the disease is migraine disorder.