Previous studies have shown that SIRT3 is closely associatedwith oxidative stress and plays a key role in cardiovascular diseases. To assess the activation of SIRT3 deacetylationby SKLB-11A in H9c2 cells, we examined the acetylationstatus of mitochondrial proteins following SKLB-11A treatment.We found that SKLB-11A induced deacetylation at K122and K68, resulting in enhanced MnSOD enzymatic activity (Figure D). Here, SOD2 is linked to cardiovascular disorder.