Our recent study investigated the effect of punicalagin on endothelial dysfunction and showed that punicalagin enhanced FoxO1 nuclear translocation and that silencing FoxO1 remarkably abolished the ability of punicalagin to augment the mitochondrial biogenesis, eNOS expression and oxidative stress, leading to amelioration of endothelial dysfunction [52]. The gene discussed is FOXO1; the disease is endothelial dysfunction.