By contrast, the inhibition (or reduction) of HDAC6, a cytoplasmic HDAC isoform that regulates microtubule behavior and stability via α-tubulin acetylation (Hubbert et al., 2002), seems to promote tau and Aβ clearance, thereby ameliorating the memory deficits in AD models (Cook et al., 2012; Sung et al., 2013; Zhang et al., 2014). Here, HDAC9 is linked to Alzheimer disease.