Others have reported HDAC-mediated modulation of epithelial to mesenchymal cell transformation and resulting suppression of fibrosis in animal models of hypertensive nephropathy with the HDAC6i, Tubastatin-A; diabetic nephropathy with the pan-HDACi, TSA; and obstructive nephropathy with MS-275 and TSA49–52. This evidence concerns the gene HDAC9 and hypertensive nephropathy.