For instance, it is known that HDAC6 is elevated in AD patients (Ding et al., 2008), and that its deletion restores the cognitive deficits observed in APPPS1-21 mouse model of AD (Govindarajan et al., 2013), but it is also known that the main effect of this protection is a consequence of the modification of tubulin acetylation (Govindarajan et al., 2013). The gene discussed is HDAC6; the disease is Alzheimer disease.