HDAC4 undergoing nuclear accumulation induces neuronal death by repressing the pro-survival factors MEF2, CREB and PPARγ (peroxisome proliferator-activated receptor γ; Bolger and Yao, 2005; Yang et al., 2011; Li et al., 2012), which have become known as the pathological causes for several disease models, such as PD, stroke, and ataxia telangiectasia (Li et al., 2012; Kassis et al., 2016; Wu Q. et al., 2017). Here, HDAC4 is linked to Stroke.