In a bovine model of mastitis (a system with noted differences from human PCM), mechanistically, exogenous CXCL12 treatment of bovine mammary epithelial cells led to a significant increase in p65 phosphorylation, suggesting that CXCL12 may trigger EMT and inhibit epithelial cell proliferation through the NF-κB pathway. This evidence concerns the gene NFKB1 and mastitis.