Moreover, high expression of HDAC9 is consistent with an increased risk of atherosclerosis.125 HDAC9 upregulation in macrophages during atherosclerosis represses cholesterol efflux and M2 polarization, and in HDAC9-deficient mice, the phenotype of macrophages switches from the proinflammatory M1 to the anti-inflammatory M2 state via PPAR-γ.108. This evidence concerns the gene PPARG and atherosclerosis.