These mechanisms include the induction of the antifibrotic factors including α and β Klotho, SIRT1, and SMAD7, suppression of profibrotic factors including TGF-β, FGF2, WNT1, and β-catenin, and inhibition of renal inflammatory mediators (TNFα, and IL-6), as illustrated in the effect of 3WJ-Kapt/anti-miR-34a in CKD mice in the current study. This evidence concerns the gene KL and chronic kidney disease.