The existence of such regulatory pathways is congruent with the significantly higher levels of TNFα, IL-1β, CXCL8 and CCL2 expression in breast tumors, as compared to normal breast cells [63], and with the ability of oncogenic RasG12V and TNFα (each alone) to up-regulate CXCL8 expression (through NF-κB activation) in tumor cells, as well as in other types of cells [33,34,36,64,65]. The gene discussed is CCL2; the disease is neoplasm.