A deficiency of MCP-1 (CCL2) or CCR2 (CCL2 receptor) in mice during obesity results in the impairment of CAMφ recruitment to adipose tissue, thus impeding the induction of insulin resistance by a high-fat diet (HFD) [64, 65] and suggesting an important role for CAMφs in T2D initiation and development (see Figure 2). This evidence concerns the gene CCL2 and type 2 diabetes mellitus.