In Gestational Diabesity, the pro- and anti-inflammatory responses loss their equilibrium and the pro-inflammatory response predominates: increased levels of leptin and TNF-α, a state of hypoxia, abnormal oxidative stress, and enhanced ROS generation result in insulin resistance in the feto-placental vasculature, while the reduced levels of adiponectin and IL-10 and increasing NO bioavailability are demonstrated in this tissue (93, 96). The gene discussed is LEP; the disease is Insulin resistance.