miR-22 was also predicted to target HDAC4; reversal of acetylation defects have been shown to ameliorate neurodegeneration in cellular and animal models of HD [13], and recent evidence has indicated that the administration of HDAC inhibitor suberoylanilide hydroxamic acid (SAHA) may work via diminishing HDAC4 expression post-transcriptionally [14]. This evidence concerns the gene HDAC9 and Huntington disease.