The mechanisms operative in this response, as derived from preclinical studies, include (1) an amelioration of hypothalamic glucose sensing neurons’ loss of responsiveness to hyperglycemia required for post meal (insulin-stimulated) glucose disposal [3]; (2) a reduction in elevated sympathetic tone to reduce hepatic and peripheral insulin resistance [2,11,13]; (3) a reduction in leptin resistance [2,11,13], and (4) a simultaneous reduction in hypothalamic overactive neuropeptide Y and corticotropin releasing hormone (CRH) functions to improve peripheral glucose disposal [14]. The gene discussed is INS; the disease is Hyperglycemia.