Hdac9–/–Apoe–/– BMMs have reduced TNF‐α‐induced up‐regulation of pro‐inflammatory gene expression, and during the development of atherosclerosis, HDAC9 binds to, deacetylates and activates inhibitory kappa B kinase (IKK)‐α and β, driving inflammatory responses in macrophages and endothelial cells.53 This evidence concerns the gene APOE and atherosclerosis.