Supplementation of IL-33 in metastatic tumors restrained tumor growth rates and frequencies of circulating tumor cells by upregulating APM and functionality of major histocompatibility complex (MHC)-molecules, indicating the inhibition function of IL-33 to primary tumors in cancer immune-surveillance and losing that function during metastatic transition as immune escape (37). The gene discussed is IL33; the disease is metastatic neoplasm.