Studies have found that the increased acetylation of very-long chain acyl-CoA dehydrogenase deficiency (VLCAD) and hydratase subunit A (HADHA) can decrease the fatty acid oxidation (FAO) of HFpEF-derived myocardial cells, and the supplementation of NAD+ can effectively reduce the FAO defect 10. This evidence concerns the gene HADHA and very long chain acyl-CoA dehydrogenase deficiency.