The deletion of Sirt6 in proximal RTECs exacerbates UUO-induced tubular injury and ECM deposition, and further studies have revealed that proximal tubular Sirt6 may play an essential role in UUO-induced tubular interstitial inflammation and fibrosis by regulating Sirt6-dependent β-catenin acetylation and ECM protein promoter transcription [155]. This evidence concerns the gene SIRT6 and inflammatory response.