Furthermore, since our microarray data (Table 1) have implicated inflammation and fibrosis as common cardinal pathogenetic mechanisms that promote diabetic nephropathy, we performed transcriptomic analysis of the fibro-inflammatory marker genes (TNFα, TGFβ, Col1a1, Ccl2, Saa3, CCAAT/ enhancer binding protein β (C/EBP β), EMR1, Macrophage-expressed gene 1 (Mpeg1), and NOX2) in the tissues of the same kidney. The gene discussed is CCL2; the disease is diabetic kidney disease.