Conversely, broad-spectrum HDAC and specific HDAC inhibitors (95–97) have been shown to rejuvenate the anti-renal fibrosis effect of Klotho by facilitating PPARγ acetylation to effectively regulate Klotho, ultimately leading to a significant restoration of Klotho protein levels and successful alleviation of renal and bone injuries associated with renal fibrosis. Here, HDAC9 is linked to renal fibrosis.