To test the extent to which AOX can functionally replace cIII + cIV in cardiomyocytes, we combined it with a second model in which heart failure is a direct result of mitochondrial cIV deficiency, brought about by cardiomyocyte-specific knockout of Cox10, a biosynthetic enzyme for heme a, an essential prosthetic group of cIV. This evidence concerns the gene COX10 and heart failure.