While upregulation of islet MT genes under diabetes may be explained by an effect of the unfavorable glucolipotoxic and proinflammatory diabetic milieu, the downregulation of islet Mt1 and Mt2 mRNA levels in compensating 6-week-old db/db mice and DIO mice, despite the presence of an evident stress signature in these islets [112,116,117], is intriguing and suggests a different regulatory mechanism and a biological role other than antioxidant defense in this context. The gene discussed is MT1A; the disease is diabetes mellitus.