Interestingly, our findings regarding the impact of FoxO1 and FoxO3a on apoptosis and autophagy (16) are in contrast to findings of previous studies conducted in different experimental settings which showed that enhancement of cardiac FoxO1 protein expression is responsible for the increased autophagy and apoptosis in mice with DCM (17), while increase in FoxO3a activation has been shown to be a mechanism by which high glucose induced oxidative stress and apoptosis in cardiac microvascular endothelial cells (18). The gene discussed is FOXO1; the disease is familial dilated cardiomyopathy.