In particular, heart-specific knockout of ZIP13 leads to CaMKII activation, mitochondrial swelling, increases the mitochondrial Ca2+, ROS production, decreases the mitochondrial respiration control rate and dissipation of mitochondrial membrane potential in a CaMKII-dependent manner, and finally, exacerbates myocardial infarction in mouse hearts subjected to I/R. The gene discussed is CAMK2G; the disease is myocardial infarction.