In this way, our data suggest that during CAC development, the global absence of IL4Rα generates an inflammatory response that favors the recruitment of M1 macrophages (F480+TLR2+STAT1+iNOS+) in the colon and that this could be associated with lower rates of tumor development through IFN-γ production by T cells which may be orchestrating tumoricidal responses, while the IL13Rα2 receptor could be promoting tissue repair processes through Arg1 and Relmα1 as a compensatory mechanism in the absence of IL4Rα. This evidence concerns the gene STAT1 and neoplasm.