In this regard, the fact that Sirt3 localized in mitochondria directly prevents mPTP opening by modulating cyclophilin D strongly suggests that Sirt3's primary action is to suppress mPTP opening and consequent mitochondrial dysfunction, and that the suppression of cardiac hypertrophy could be secondary to the suppression of mitochondrial/cardiac dysfunction [2]. Here, SIRT3 is linked to cardiac hypertrophy.