Treatment of mice challenged with STZ with hrANXA1 (weeks 1–13) did not alter the diabetic phenotype (reduced insulin levels, elevated blood glucose and impaired OGTT), but attenuated the cardiac dysfunction and the proteinuria caused by diabetes, suggesting that hrANXA1 reduces the cardiac and renal injury caused by hyperglycaemia and excessive oxidative stress (organ protection rather than reduction of diabetes). This evidence concerns the gene INS and Hyperglycemia.