In current study, we demonstrated that, in gastric cancer cells, SIRT3 interacts with and deacetylates LDHA, causing increased LDHA activity; and SIRT3 overexpression leads to increased cellular ATP production and MnSOD activity paralleled with reduced cellular ROS level, indicating an increased oxidative scavenger ability of SIRT3 possibly via deacetylation-mediated MnSOD enzyme activation. Here, SOD2 is linked to gastric cancer.