One possible explanation might be that instead of an alteration of the basal levels of histone acetylation, AD might be more related with the incapacity of modifying the epigenetic patterns in certain conditions, such as learning and memory formation, in which HDAC inhibitors that increase histone acetylation would “prime” the levels of histone acetylation and consequently, of gene activity (Gräff and Tsai, 2013a,b; Gräff et al., 2014). Here, HDAC9 is linked to Alzheimer disease.