There is no contradiction between our finding of downregulation of Slc25a5, one of the genes responsible for pumping in Ca2+, and recent reports of mitochondrial Ca2+ overload during the acute phase of the myocardial ischemia-reperfusion [87] because in the post-ischemic failing heart (our case), mitochondrial Ca2+ content is lower [88]. The gene discussed is SLC25A5; the disease is myocardial ischemia.