In DKD, various immune cell populations1 and several circulating cytokines have been correlated with poor cardiorenal outcomes and mortality, including neutrophils,2 eosinophils,3 CD4+ T cells,4 IL-1 α/β, IL-6, C-reactive protein (CRP), TNF α, TNFR1/2, and CCL2.5, 6, 7, 8, 9, 10, 11, 12, 13, 14 The distribution of risk associated with these biomarkers has indicated that inflammation plays a clinically relevant, disease-modifying role in at least 20% to 40% of patients with DKD.1 This evidence concerns the gene CCL2 and diabetic kidney disease.