NFKB1 and neoplasm: Moreover, in several anatomic sites chronic inflammation is crucially implicated in tumor initiation, producing a mutagenic environment through the release of reactive oxygen/nitrogen species from infiltrating immune cells, generating cytokines, chemokines, growth factors, and anti-apoptotic proteins, and activating tumor-stimulating signaling pathways (e.g., NF-kB, p38MAPK, STAT3) (42, 47–49).