In fact, MCUb can be described as a protective gene in cardiac myocytes since i) its expression is transiently induced after ischemia-reperfusion injury and ii) transgenic mice overexpressing MCUb have a reduced mitochondrial Ca2+ uptake ability, thus preventing Ca2+ overload, which is sufficient to protect myocytes from ischemia-reperfusion injury and to decelerate their ongoing necrosis [72,73]. Here, MCUB is linked to ischemia.