Moreover, miR-200c and miR-200a have been recently associated with cardiac hypertrophy in animal models [45–47]; further, both miR-200c and miR-200a target SIRT1 [25, 53], and in addition, we demonstrated that miR-200c targets eNOS, contributing to endothelial dysfunction establishment increasing ROS and decreasing NO, that is a potent vasodilator necessary for endothelial function preservation [59]. The gene discussed is SIRT1; the disease is endothelial dysfunction.