Genetic knockdown and pharmacologic inhibition of MCP-1/CCL2 already demonstrated to attenuate inflammation, tubulus atrophy, albuminuria, and progressive fibrosis in several animal models of diabetic and non-diabetic kidney disease (Boels et al. 2017; Chow et al. 2006; Giunti et al. 2010; Kitagawa et al. 2004; Tarabra et al. 2009). Here, CCL2 is linked to diabetic kidney disease.