One interpretation of these opposed effects is that in the absence of IL-1R8, an exacerbated inflammatory response (bringing into play the different cell types sensitive to IL-18/IL-33 and IL-37) favors solid tumorigenesis and tissue lesions during infections, while censoring of cancers in liver, particularly hepatic metastases, is partially counteracted by IL-1R8. Here, IL1RAPL1 is linked to infection.