Recent studies by two distinct groups have demonstrated that neuron-specific over-expression of HDAC2 impaired memory formation in adult mice, whereas HDAC2 deficiency resulted memory facilitation, similar to that induced by the treatment with nonselective HDAC inhibitors, suggesting that HDAC2 inhibition may be a useful strategy in the treatment of some cognitive impairments associated with psychiatric diseases [22,23]. This evidence concerns the gene HDAC2 and Cognitive impairment.