Studies have shown that dysregulation of several mediators, including nitric oxide, tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6), endothelin-1, and nicotinamide adenine dinucleotide phosphate (NADPH) oxidase, can blunt the normal sympathetic response to infection, leading to increased parasympathetic tone and a paradoxically low heart rate despite fever [6]. The gene discussed is IL6; the disease is infection.