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. The gene discussed is HDAC9; the disease is urogenital neoplasm.