In addition, the fact that therapy with MC1568 was able to reduce EndMT and favorably alter plaque phenotype with established atherosclerosis (after 10 weeks of high-fat feeding in ApoE–/– mice) is of translational importance, as it argues for the possibility that therapies targeting EndMT via HDAC inhibition may favorably affect atherosclerosis in humans with established disease. The gene discussed is HDAC9; the disease is atherosclerosis.