Our major findings showed that the whole-body deletion of Ccr2 (Ccr2−/− mice) and chimeric mice lacking Ccr2 only from bone marrow-derived cells in mice resulted in the inhibition of diabetes-induced increases of retinal superoxide, upregulation of proinflammatory genes (Inos and Icam1), leucostasis, leucocyte- and monocyte-mediated cytotoxicity against retinal endothelial cells, and most importantly, retinal capillary degeneration. This evidence concerns the gene CCR2 and diabetes mellitus.