IL1B and neoplasm: The activated STAT3 results in dimerization of the STAT3, which translocates to the nucleus and binds promoter regions of target genes, leading to secretion of pro-inflammatory factors and acute-phase proteins (e.g. IL-1β, IL-8) and resulting in an anti-apoptotic state of the cell inducing cell survival (cyclin D1, MYC, Bcl-xL and survivin) [29, 31, 39], angiogenesis (VEGF) and invasion (matrix metalloproteases) [29], and secreting immunosuppressive factors (IL-10, TGFβ and VEGF) [28, 29] increasing chances for completing the cell cycle and cell and tumor growth [30, 31, 40–43].