We include the Apcmin model of familial adenomatous polyposis, the AOM-DSS model of inflammation-driven colorectal cancer, and a model of invasive, metastatic colorectal adenocarcinoma generated by endoscope-guided orthotopic implantation of CRISPR/Cas9-engineered tumoroids with oncogenic Apc, Trp53, Kras, and Smad4 (APKS) mutations into the colonic mucosa of syngeneic mice. This evidence concerns the gene SMAD4 and Familial adenomatous polyposis.