HDAC3 overexpression or inhibition in renal epithelia was inversely related to Klotho levels, and HDAC3 was inducibly associated with transcriptional regulators NCoR and NF-κB and bound to Klotho promoter in fibrotic kidney, reinforcing that aberrant HDAC3 targets Klotho and inhibits its transcription in renal fibrosis 27. This evidence concerns the gene KL and renal fibrosis.