Chronic inflammation, as one of the main factors in the progression of diabetes and its complications, causes tissue damage and leads to the generation of new vascular structures via oxidative stress, apoptosis, endothelial dysfunction, and fibrosis (Wang et al. 2014a, b, c), (Liu et al. 2014; Li et al. 2018a, b, c) reported elevated levels of proinflammatory (TNF-1α, MCP-1), aortic fibrosis (CTGF, TGF-β1), apoptosis (caspase-3), and oxidative stress (3-nitrotyrosine (3-NT), 4-hydroxynoneal (4-HNE)) markers in the aorta of diabetic mice. The gene discussed is CCL2; the disease is diabetes mellitus.