Accordingly, in mouse models of colorectal cancer (CRC), heterozygous genetic deletion of IFNγ (Ifng+/-), homozygous deletion of the corresponding receptor (Ifngr1-/-), or antibody-mediated neutralisation of IFNγ, increased adenocarcinoma development [24, 41, 50]. This evidence concerns the gene IFNG and colorectal carcinoma.