Despite observations that SOD2, the mitochondrial-specific antioxidant enzyme that dismutates O2●− to H2O2, is upregulated in patients with type 2 diabetes mellitus [67], studies failed to show significant alterations in platelet function or thrombotic susceptibility with platelet-specific knockouts of SOD2 in non-aged non-diabetic murine models [68]. The gene discussed is SOD2; the disease is type 2 diabetes mellitus.