In the early phases of T1D development exposure of β-cells to these cytokines is thought to induce β-cell dysfunction and the expression of chemokines and cytokines, such as Ccl2 (Mcp-1), Ccl20 (Mip-3α), and Cxcl10 (Ip-10) that increase the infiltration of the islets by immune-cells [3–8]. This evidence concerns the gene CCL2 and type 1 diabetes mellitus.