Aberrations in the metabolism of diabetes lead to the excess production of mitochondrial superoxide, which is the foremost intermediary of tissue damage in diabetes, leading to the stimulation of five pathways involved in the complications of pathogenesis and deactivation of two anti-atherosclerotic enzymes, endothelial nitric oxide synthase (eNOS) and prostacyclin synthase. The gene discussed is PTGIS; the disease is diabetes mellitus.