IL1B and cancer: The classical activation pathway (M1) prevails in the presence of Th1 following response to microbial stimuli in the presence of cytokines, IFNγ and TLR ligands and results in release of additional inflammatory cytokines (IL-1b, IL-6, IL-12 and TNF-a) from macrophages, thereupon further enhancing Th1-mediated immune response and cytotoxic activity towards cancer cells, by producing high amounts of toxic intermediates, such as reactive oxygen species (ROS) and nitric oxide (NO) [64,66].