For example, despite no basal differences were found in mitochondrial respiration between Akap1-/- and wt hearts, following myocardial infarction, Akap1-/- mice exhibited increase levels of cardiac ROS and more prominent alterations in mitochondrial morphology compared to wt controls (Schiattarella et al., 2016). This evidence concerns the gene AKAP1 and myocardial infarction.