Very recently, diabetes-induced myelopoiesis, monocytosis, neutrophil production of S100A8/S100A9 and impaired lesion regression were found to be prevented by the increased levels of HDL in a human APOA1 transgenic mouse model (47), suggesting that diabetes-induced monocytosis and hampered lesion regression can be prevented by increasing cholesterol efflux from myeloid cells and their bone marrow progenitors. This evidence concerns the gene S100A8 and diabetes mellitus.