On the other hand, in cardiac vascular endothelial cells, the AMPK-Akt signal was activated to phosphorylate FOXO1 and then weakened its activity, leading to a marked elevation in the gene expression of downstream eNOS and, thus, alleviating vascular oxidative stress, which helps to improve the diastolic function of cardiac vessels in DCM. This evidence concerns the gene AKT1 and familial dilated cardiomyopathy.