Although the observed hyperglycemia and compromised insulin action might be due to activated production of catecholamines and cortisol in response to infarct extension and myocardial dysfunction, Choi et al. [33] showed that the proportion of abnormal glucose tolerance kept similar at admission and 3 months after discharge when the effects of acute stress and inflammation should have already been lessened. The gene discussed is INS; the disease is Hyperglycemia.