Specifically, IL-11 activates STAT3 phosphorylation, which inhibits IFNγ-induced STAT1 phosphorylation, thereby downregulating MHC-I and CXCL9 expression in tumor cells and impairing CD8+ T cell infiltration—promoting immune evasion and tumor growth in CRC [103]. This evidence concerns the gene CXCL9 and neoplasm.