It is noteworthy that the CAG140 knock-in mice display only a mild neurological HD phenotype as compared to R6/2 transgenic mice; this difference in phenotype may explain the discrepancy between our results in these two HD mouse models. Further, our study was largely based on evaluation of HDAC protein levels by western blotting; although this method was sufficiently sensitive to allow us to measure differences of >15-20% in R6/2 animals, it might not have permitted detection of more subtle changes in expression levels over time. This evidence concerns the gene HDAC9 and Huntington disease.