These cardiac abnormalities include left ventricular (LV) diastolic dysfunction as well as LV hypertrophy and fibrosis,9 and these changes are associated with increased cardiac oxidative stress and inflammation.10 We recently showed that activation of glucocorticoid–GR signaling may contribute to the pathophysiology of MetS and its associated complications in DS/obese rats.11 The role of the glucocorticoid–GR system in the effects of chronic stress on cardiac and adipose tissue pathology associated with MetS has remained unclear, however. The gene discussed is NR3C1; the disease is metabolic syndrome.