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. This evidence concerns the gene APOE and atherosclerosis.