Indeed, the differences in mechanisms underlying HAT/HDAC contribution to AD, PD, HD, and ALS, along with the varying types of histone acetylation alterations in different subregions of the brain and at various stages of disease progression observed in the multiple types of NDs, highlight the inadequacy of a one-size-fits-all therapeutic strategy. This evidence concerns the gene HDAC9 and amyotrophic lateral sclerosis.