In experimental and human renal diseases, the renal activation of the NF-κB pathway is associated with the overexpression of proinflammatory mediators, as initially described in human biopsies of diabetic nephropathy patients, showing colocalization of activated NF-κB and upregulation of CCL2 mRNA expression levels (Mezzano et al., 2004). The gene discussed is NFKB1; the disease is diabetic kidney disease.