Work with genetically engineered mouse models and organoids suggested that the three most common tumor-promoting events in CRC, disruption of the Apc and Trp53 tumor suppressor genes in conjunction with oncogenic mutations in Kras, suffice to induce invasion and metastatic disease [16–19], but it was not determined whether the experimental models recapitulated the particular type of invasion observed in CRC tissue specimens. The gene discussed is APC; the disease is neoplasm.