Not only does the combination therapy of ACE–I and AcSDKP strikingly suppresses renal fibrosis in diabetic CD–1 mice, but also oral administration with AcSDKP alone attenuates renal fibrosis via suppressing EndMT (Nagai et al., 2014; Nitta et al., 2016), suggesting that AcSDKP could become a potent therapeutic agent to prevent tissue fibrosis in diabetes. This evidence concerns the gene TMSB4X and diabetes mellitus.