Furthermore, the mechanism through which iNOS and its product nitric oxide influence CRC development in mice harboring mutations in the adenoma polyposis coli gene (APCMin/+) is controversial [29], [30], [31] prompting us to examine its role specifically in the context of APCMin/+Msh2−/− mouse model of CRC. The gene discussed is NOS2; the disease is colorectal carcinoma.