Recent studies reported that Klotho suppression after acute kidney injury involved the HDAC1/2-associated pro-inflammatory signaling20 and Klotho repressions incurred by the promoter hypermethylation in patients and animal studies of CKD30, 31 are presumably mediated by a transcription repression mechanism requiring HDAC activities, raising the possibility that inhibition of HDAC might relieve Klotho repression and restore its renal protective capacities. This evidence concerns the gene KL and urogenital neoplasm.