It was concluded that EMPA inhibits myocardial fibrosis partly through the inhibition of collagen formation and deposition via the classical transforming growth factor-β (TGF-β) and downstream Smad pathway and decreases oxidative stress via promoting nuclear erythroid 2-related factor 2 (Nrf2) translocation to the nucleus and activating Nrf2/antioxidant response element (ARE) signaling in the T2DM KK-Ay mice model [22]. The gene discussed is NFE2L2; the disease is type 2 diabetes mellitus.