Of particular interest are the results obtained in R6/2 mice, a model for Huntington’s disease (HD) with CAG repeat expansions in Huntingtin (HTT) gene, in which SAHA treatment reinstates transcriptional repression—via global histone acetylation [15]—and reduces HTT-expanded aggregates with the restoration of BDNF levels in the cortex [58]. This evidence concerns the gene HTT and juvenile Huntington disease.