In the acute phase, cutaneous immunological mechanisms underlying CRPS have been discovered, including autoimmunity [5], keratinocyte activation, proliferation, and expression of inflammatory mediators such as tumor necrosis factor alpha (TNFα), interleukin-1 beta (IL-1β) and interleukin-6 (IL-6), nerve growth factor (NGF), and mast cell activation [6, 7]. The gene discussed is IL6; the disease is complex regional pain syndrome.