Inhibitors of HDACs, such as trichostatin (TSA) and vorinostat, and HDAC knockdown by small interfering RNAs have been effective in alleviating ECM degradation and cartilage degeneration during OA progression.64–69 Furthermore, several siRNAs against HDAC have been approved by the Food and Drug Administration (FDA) in the US for cancer treatment, including vorinostat, romidepsin, valproate and depakote.66 Further investigation is needed to determine if HDAC siRNAs could be used for OA treatment. This evidence concerns the gene HDAC9 and cancer.