Serum levels of IL-17, interferon (IFN)-γ, and TNF-α were elevated, accompanied by increased intra-tumor accumulation of activated natural killer (NK) cells and CD8+T cells, suggesting that loss of IL-33 signaling through the ST2 receptor can promote Th1/Th17 polarization of the innate and acquired immune responses [51,52]. This evidence concerns the gene IL33 and neoplasm.