The pivotal role of p66Shc in bone marrow-derived cells, the co-localization of p66Shc with macrophages, and the expression of pro-atherogenic (CD36) and pro-inflammatory (NF-κB p65, IL-6, and TNFα) genes in hyperglycaemia-associated macrophages are entirely congruent with the previously proposed pathogenetic function of macrophages in diabetes-associated atherosclerosis in animal36–38 and clinical studies39. This evidence concerns the gene NFKB1 and diabetes mellitus.