Recent experimental evidence indicates that Ca2+ handling at mitochondrial level is more tightly controlled by the balance between molecules that stimulate mitochondrial Ca2+ uptake and molecules that inhibit Ca2+ uptake.10 Specifically, the mitochondrial Ca2+ uniporter (MCU) is the major molecule stimulating mitochondrial Ca2+ uptake.11 With an in vivo MI/R model, Luongo et al.12 revealed that MCU deficiency conferred resistance to IR injury by preventing mitochondrial Ca2+ overload. Here, MCU is linked to myocardial infarction.