In these studies, CGRP is found to be released from trigeminal ganglia neurons, its transcription increases under conditions imitating neurogenic inflammation, and migraine pharmacotherapies can both inhibit CGRP transcription and reduce CGRP release, and tumor necrosis factor-α (TNF-α), an endogenous inflammatory mediator involved in migraine, can arouse CGRP transcription [9]. This evidence concerns the gene TNF and migraine disorder.