In addition, NAD+ production by the NNT enhance SIRT3-mediated deacetylation and loss of NAD+-dependent deacetylase SIRT3 increases the acetylation of IDH2 at K413 and decreases its enzymatic activity by reducing dimerization, thus regulates mitochondrial redox status and promotes cell tumorigenesis in luminal B breast cancer,137 and B cell malignancies.138 SIRT5-mediated IDH2 desuccinylation also regulates cellular NADPH homeostasis and redox potential.54 The gene discussed is IDH2; the disease is breast cancer.