[8] Generally, HDAC2 is considered a putative target for the treatment for a variety of diseases, due to its involvement in cell cycle progression.

The metallic ion facilitates the nucleophilic attack of the carbonyl group by a coordinated water molecule, leading to the formation of a tetrahedral intermediate.

This intermediate is momentarily stabilized by hydrogen bond interactions and metal coordination, until it ultimately collapses resulting in the deacetylation of the lysine residue.

[14] The HDAC2 active site consists of a lipophilic tube which leads from the surface to the catalytic center, and a 'foot pocket' containing mostly water molecules.

Thus, it plays an important role in transcriptional regulation, cell cycle progression and developmental events.

[18] Furthermore, a recent study found that inhibition of HDAC2 via c-Abl by tyrosine phosphorylation prevented cognitive and behavioral impairments in mice with Alzheimer's disease.

[19] The results of the study support the role of c-Abl and HDAC2 in the signaling pathway of gene expression in patients with Alzheimer's disease.

A recent study discovered decreased metastasis formation in mouse models that develop pancreatic cancer when the murine ortholog Hdac2 was genetically depleted.