In a mouse model of colitis-associated cancer, genetic IL-4-deficiency (thus removing endogenous IL-4 signals) reduced tumour burden [132], and genetic deletion of STAT6, the downstream signaling mediator for IL-4, similarly reduced tumorigenesis in a model of adenomatous polyposis coli (APC)-mutation-mediated CRC [133]. This evidence concerns the gene IL4 and neoplasm.