Although the activation of IL-1β is necessary to resolve acute inflammation processes, the sustained release of IL-1β in obesity maintains both a constant activation of pro-inflammatory cascades [43] as well as an enhanced expression of pro-tumorigenic mediators including nitric oxide (NO), cyclooxygenase-2 (COX-2), chemokines and metalloproteinases (MMPs) [53] favoring tumor development [12]. This evidence concerns the gene PTGS2 and neoplasm.