CSCs, namely those rare immortal cells of the tumor bulk with the capacity for self-renewal, multipotency, tumorigenicity, and quiescence (90), proliferate in response to activation of the NF-kB and STAT3 pathways (91), and EMT, a prerequisite for invasiveness, is favored by exposure of tumor cells to TNF-α, IL-6, and TGF-β (92, 93). Here, NFKB1 is linked to neoplasm.