Considering carotid body-mediated mechanisms of obesity-related sympathoactivation, insulin and leptin seem to be of particular relevance since obesity is usually accompanied by hyperinsulinemia and hyperleptinemia [12], and both, insulin and leptin have been shown to exert sympathoexcitatory effects via direct action on the carotid bodies in animal models [13–16]. The gene discussed is INS; the disease is Hyperinsulinemia.