Previous studies show that angiotensin II (ANG II), angiotensin II type 1 receptor (AT1-R), proinflammatory cytokines (PICs), NAD(P)H oxidase, and nuclear factor-kappa B (NF-κB) all appear to be potential targets for PVN interventions that might substantially reduce the adverse peripheral effects of sympathetic nerve activity and neurohumoral regulation in heart failure. The gene discussed is NFKB1; the disease is heart failure.