HDAC3 and cardiovascular disorder: Furthermore, myeloid-specific HDAC3 knockout promotes collagen deposition in atherosclerotic lesions and directly increases the acetylation of TGF-β1, driving the transformation of macrophages toward a profibrotic phenotype and an anti-inflammatory phenotype, suggesting that HDAC3 may serve as a potential novel therapeutic target for cardiovascular diseases (Hoeksema et al., 2014).