Treatment of either TSA or another HDAC inhibitor, suberonylanilide hydroxamic acid (SAHA) targeting HDAC I in MRL/lpr lupus-prone mice showed reduced proteinuria, glomerulonephritis, spleen weight, and mesangial cell inflammation, associated with an increased accumulation of acetylated histones H3 and H4 in total cellular chromatin [106,107]. The gene discussed is HDAC9; the disease is systemic lupus erythematosus.