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Oxidative stress is one of the causes of aging and other diseases. Nrf2 is the main transcription factor regulating antioxidant gene expression. In recent years, it has been found that inhibiting Nrf2 activity or increasing oxidative pressure can replicate premature aging defects, and reactivating Nrf2 activity can reverse nuclear aging defects and restore cell vitality. SIRT6 is one of the few proteins that can regulate life span and aging at the same time. SIRT6 gene deficient mice show degenerative changes similar to human premature aging 3 weeks after birth and eventually die. SIRT6 deficient cells show the characteristics of accelerated aging, while the deletion of SIRT6 in human cells does not directly lead to the damage of genetic material in the nucleus and genomic instability, but significantly reduces the antioxidant capacity of cells and causes the accumulation of intracellular reactive oxygen species and DNA oxidation products. At present, the interaction between Nrf2 and SIRT6 protein and its mechanism are not clear. In this study, yeast two-hybrid and tag pulldown methods were used to analyze the protein interaction domain between Nrf2 and SIRT6. The experiment found that SIRT6 directly interacts with Nrf2, SIRT6 Interacts with the Neh1 and Neh3 domains of Nrf2.