As such, the findings that HDAC6 expression and/or activity is increased in primary hippocampal neurons treated with Aβ(1–42) (21), as well as in animal models and patients with AD (21, –, 23), may suggest that Aβ-mediated stimulation of HDAC6 activity promotes KXGS deacetylation, leaving these motifs exposed and vulnerable to phosphorylation. This evidence concerns the gene HDAC6 and Alzheimer disease.