Arguments supporting the theory that neurogenic inflammation may play a role in triggering CRPS-1 are higher concentrations of bradykinin, neuropeptide Y, Calcitonin Gene-Related Peptide (CGRP) and vasoactive intestinal peptide in patients with CRPS-1 [17] and protein extravasation induced by substance P [18]. The gene discussed is TAC1; the disease is complex regional pain syndrome type 1.