Of note, the cardioprotective effects of chaetocin was also dependent on SIRT1 since Sirt1 depletion (Fig. 10) or inhibition (Supplementary Fig. 31) abrogated the reduction of infarction size, the normalization of heart function, the changes in anti-oxidant gene expression, and the suppression of ROS levels induced by chaetocin in post-MI mice. The gene discussed is SIRT1; the disease is myocardial infarction.