Furthermore, disturbance of the cellular milieu generated by the byproducts of inflammation exacerbates genome instability that promotes the neoplastic disease’s plasticity to expedite tumorigenesis and precipitate multiple hallmarks. Generally poised as the activator of procaspase-1, inflammasomes are cytosolic multi-protein complexes that predominantly engage with innate immunity defense via activation of pro-interleukin (IL)-1β and pro-IL-18 cytokines (4). This evidence concerns the gene IL1B and neoplasm.