Deletion of histone deacetylase HDAC9 in an atherosclerosis mouse model (LDLr−/−, low density lipoprotein receptor knock out) reduced atherosclerosis and resulted in polarization of macrophages toward M2-like phenotype as well as upregulation of lipid homeostatic genes and downregulation of inflammatory genes (41). This evidence concerns the gene LDLR and atherosclerosis.