The CDs/y strain that is fed DD and phenotypically develops diabetes generates, therefore, a higher level of oxidative stress that is poorly dealt with by the antioxidative defenses – in the face of inadequate disposal of reactive oxygen species (ROS) by detoxifying enzymes such as SOD1 and SOD2, and the imbalance between production and detoxification that determines the intracellular ROS concentration (Hasnain et al., 2016) – leading to development of diabetes. This evidence concerns the gene SOD1 and diabetes mellitus.