In an experimental murine model of myocardial infarction,[24] Dadabayev et al found that ligation of the left anterior descending coronary artery resulted in a significantly larger infarct size in ApoA1-null (ApoA1−/−) mice than in ApoA1 heterozygous (ApoA1+/−) mice, and that the pathology was traced to a functional defect in mitochondrial electron transport that arose from a deficiency in the CoQ10 pool of ApoA1-null mice. This evidence concerns the gene APOA1 and myocardial infarction.