Furthermore, transgenic mice overexpressing SDF-1α with in β-cells (RIP-SDF-1 mice) could resistant to STZ-induced β-cell apoptosis and diabetes through activating the Akt protein kinase, while SDF-1α receptor antagonist AMD3100 induced apoptosis in MIN6 β-cells (33), suggesting that upregulation of SDF-1α in islets may represent a defense system against β-cell injury. Here, CXCL12 is linked to diabetes mellitus.