In addition, the aberrant MAP4 phosphorylation-induced cardiomyocyte mitochondrial dysfunction was still noted in vivo experiments and in heart tissues of patients of tetralogy of Fallot, and the MAP4 phosphorylation mutant mice developed cardiomyopathy at the age of 30–34 and 70–74 weeks, which mitochondrial dysfunction is deemed an important trigger for myocardial impairment and cardiac dysfunction [9]. This evidence concerns the gene MAP4 and Tetralogy of Fallot.