The pleiotropic effects of cytokines in tumorigenesis can explain the cross-talk among the pathways that regulate tumor progression, such as Janus kinase (JAK)/STAT, PI3K, AKT, Rac, MAPK, nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB), cFos and mammalian target of rapamycin (mTOR) [46]. This evidence concerns the gene NFKB1 and neoplasm.