Therefore, although our previous study has revealed that HDAC3-miKO did downregulate PU.1 expression, which was proved to be responsible for gene regulation induced by HDAC3-miKO 30, the elevation of CCL7 expression in this study suggested another regulatory mechanism independent of PU.1 in HDAC3-miKO after stroke, which needs further investigation. This evidence concerns the gene HDAC3 and stroke disorder.