In endotoxemia, the stimulation of vagus nerve attenuated systemic TNF levels in animals with α7nAChR deficiency in the nervous system, but failed in animals with an α7nAChR deficient immune system (30), identifying the α7nAChR expressed on macrophages and other immune cells as a main mediator of CAP output (28). This evidence concerns the gene CHRNA7 and serum lipopolysaccharide activity.