Increased levels of IFN-γ, IL-17, IL-9, IL-6, IL-1β, CCL2 (MCP1), CCL4, and CXCL10 (IP-10) (3–6, 15, 17), as well as activation and phenotypic plasticity of Th17 cells have been associated with the development of islet autoimmunity and progression from the autoantibody-positive state towards clinical type 1 diabetes (18, 19). This evidence concerns the gene CCL2 and type 1 diabetes mellitus.