Physiologic adaptative mechanisms to anemia, such as increases in cardiac output, 2,3-diphosphoglycerate levels (decreasing Hb oxygen–binding affinity), tissue oxygen extraction, and redistribution of regional blood flow in favor of coronary and cerebral circulation, may not have sufficient time to occur and sustain tissue oxygen delivery in acute anemia.23 In the context of acute MI, the additional myocardial oxygen consumption caused by the required acute increase in cardiac output may further worsen clinical outcomes. Here, GSTM1 is linked to anemia.