In accordance with this hypothesis, the selective class IIa HDACs inhibitor, MC1568, caused the binding of HDAC9 to SUMO1 with a consequent degradation of this deacetylation factor in cortical neurons after OGD/Rx, as far as to other HDAC class IIa members 29, 45, and exerts a neuroprotective effect after stroke 39. Here, HDAC9 is linked to stroke disorder.