An increase of CK2α expression and inflammatory cell infiltration in a murine glomerulonephritis model has also been reported to lead to increases in production from genes in the ERK pathway (c-fos, Egr-1, and Elk-1), NF-κB-regulated inflammatory cytokines (TNF-α and MCP-1), and extracellular matrix proteins (collagen, fibronectin, TGFβ, and PDGF)32. This evidence concerns the gene CCL2 and glomerulonephritis.