These results are consistent with studies on HDAC6 knockout mice, a class II HDAC known to target K40 acetylation of α-tubulin, demonstrating that although these mice display a significant increase in tubulin acetylation in the brain, this phenomenon does not rescue disease progression in a mouse model of Huntington's disease [64], [65], [66]. The gene discussed is HDAC9; the disease is juvenile Huntington disease.