Based on the above understanding that infiltrated macrophages predominantly occurred in the infarct core where myelin debris surged and that HDAC3-deficient microglia have summoned additional macrophage reinforcements, we hypothesized that HDAC3-miKO could accelerate myelin debris clearance by boosting macrophage recruitment, in this way promoting oligodendrogenesis and improving long-term histological and functional integrity of white matter after stroke. The gene discussed is HDAC3; the disease is Stroke.