A significant increase in the expression of NF-κB/p65 in infected IBC carcinoma tissue may be due to the secondary involvement of biological molecules such as cytokines and chemokines that characterize IBC tumor biology, but which could be elevated due to HCMV infection of immune cells, fibroblasts or epithelial cells, and in which HCMV induces oncomodulatory proteins through activating NF-κB/p65 signaling pathways [55]. The gene discussed is NFKB1; the disease is neoplasm.