The predicted activation of MYC and ZEB1, both subject to miRNA-mediated regulation, highlights their central roles as modulators of mitochondrial metabolism and cellular plasticity following myocardial infarction [44,45] Moreover, locally produced IL6 amplifies mitochondrial dysfunction via STAT3-dependent signaling, exacerbating ROS generation and impairing oxidative phosphorylation in cardiomyocytes [46]. This evidence concerns the gene MYC and myocardial infarction.