However, in our model of early diabetes, only moderate tissue inflammation was documented, mainly characterized by the increased expression of the monocyte chemoattractant protein-1 (MCP-1) and fractalkine, in both cardiomyocytes and fibroblasts [10], while more severe tissue and systemic inflammation occur in the advanced stages of diabetic cardiomyopathy, as well as in other dysmetabolic pathologies [52]. The gene discussed is CCL2; the disease is diabetic cardiomyopathy.