Collectively, our findings strongly support the notion that the activation of CYP4A/20-HETE plays a pivotal role in the pathogenesis of diabetic kidney disease (DKD), and that the renoprotective effects of dapagliflozin, an SGLT2 inhibitor, are mediated via the inhibition of CYP4A/20-HETE. This evidence concerns the gene SLC5A2 and diabetic kidney disease.