Therefore, knowing that leptin, proinflammatory cytokines, and insulin augment sympathetic nervous system activity, that the CB integrates its action centrally via the modulation of sympathetic activity, and that the CB possesses receptors for all these mediators, we hypothesize that hyperleptinemia, proinflammatory cytokines, and hyperinsulinemia are mediators that contribute to the CB dysfunction that contributes to the genesis of metabolic diseases (Figure 2). The gene discussed is INS; the disease is Hyperinsulinemia.