In addition, SIRT3 overexpression suppressed NF-κB-dependent transcriptional activity of inflammatory genes, decreased phosphorylation of ERK1/2 and p38, and decreased ROS levels, indicating a possible molecular mechanism of SIRT3-mediated antioxidant and anti-inflammatory effects in proximal tubular cells (Koyama et al., 2011).SIRT3 deficiency has been reported to promote mesenchymal transformation of tubular epithelial cells, thereby inducing fibrosis in DKD (Sriyastava et al., 2021). The gene discussed is SIRT3; the disease is diabetic kidney disease.