Despite the considerable reductions in enzymic antioxidant expression/activities accompanying impaired bone healing with T2DM (16, 17, 19, 127–135), few studies have evaluated the potential delivery of exogeneous enzymic antioxidants to hyperglycaemic bone defects, via strategies such as gene therapy, SOD/catalase and GPx mimetics (Salens and Ebselen, respectively) and nanozymes, or recombinant protein approaches, in order to alleviate oxidative stress-induced inflammation, cell/tissue damage and impaired bone healing; unlike other T2DM-related complications (194–202). The gene discussed is SOD1; the disease is type 2 diabetes mellitus.