After the restoration of AcSDKP levels in diabetic CD-1 mice, the mice displayed suppressed AcSDKP levels, inhibited renal fibrosis in fibrotic kidney involved concomitant reduction in the DPP-4-associated increase in the mesenchymal activation program, suggesting that the suppression of the endogenous antifibrotic peptide AcSDKP is a therapeutic target for combating kidney fibrosis. This evidence concerns the gene TMSB4X and renal fibrosis.