Similarly, HDAC4 and HDAC5 increased a cell viability through an inhibition of HMGB1, a central mediator of tissue damage following acute injury and it has been shown that NADPH oxidase-mediated HDAC4 and HDAC5 expression contributed to the cerebral ischemia injury through the HMGB1 signaling pathway that could be an effective therapeutic target to treat stroke (He et al., 2013). This evidence concerns the gene HDAC4 and Stroke.