Mechanistically, compared with non-diabetic WT mice, the degree of the phosphorylation of mitogen-activated protein kinases (MAPKs) p38, c-Jun N-terminal kinase (JNK) and extracellular signal-regulated kinase (ERK) was significantly higher in non-diabetic Anxa1−/− mice in both the heart and kidney, and was further enhanced after STZ-induced type 1 diabetes. Here, ANXA1 is linked to type 1 diabetes mellitus.