Human atherosclerotic plaque macrophages and BMDMs, in the presence of diabetes, showed DE of RUNX1-regulated genes, including several previously linked to inflammation and atherosclerosis.49,50 Our work extends that of Alrdahe and colleagues,61 who recently showed that diabetes-derived human macrophages cultured for 6 days in vitro maintain a proinflammatory priming and hyperpolarize to a proinflammatory phenotype when stimulated with LPS and IFN-γ or tumor necrosis factor-α. The gene discussed is TNF; the disease is diabetes mellitus.