The model employs two distinct pathological mechanisms: a selective inhibition of glucose-stimulated insulin secretion through a specific inhibition of glucokinase, and an induced formation of reactive oxygen species (ROS) that promote selective necrosis of pancreatic beta cells; both effects are related to the chemical properties and structure of alloxan, collectively resulting in a pathophysiological state of diabetes [46,47,48]. This evidence concerns the gene INS and diabetes mellitus.