Considering that mitochondrial ultrastructure and ADP-dependent respiratory capacity (data not shown) remained intact in the affected tissue during NSTE-ACS, the observed suppression of oxygen consumption likely reflects the shift from aerobic to glycolytic ATP production that characterizes myocardial stunning in the context of ischemia, which is regulated by HIF-1α and CaMKII in response to changes in tissue oxygen [31] and calcium [32], respectively. The gene discussed is HIF1A; the disease is ischemia.