Previous studies have indicated that VN electric-stimulation during septic shock [16] and endotoxemia [14] specifically attenuates TNF production in spleen macrophages (main source of TNF in endotoxemia) through the cholinergic anti-inflammatory pathway [14], which is dependent on the anatomical and functional integrity of the VN, celiac-superior mesenteric plexus ganglia, and the splenic nerve [14]. This evidence concerns the gene TNF and septic shock.