Central TNF-α inhibition reduced the expression of angiotensin type 1 receptor (AT1R), NADPH oxidase, TNF-α and IL-1β, increased the expression of neuronal and endothelial nitric oxide synthase, and reduced production of reactive oxygen species (ROS) in the PVN; central TNF-α inhibition simultaneously decreased plasma norepinephrine levels and reduced cardiac dysfunction in heart failure rats [14]. The gene discussed is TNF; the disease is heart failure.