Several rodent models of CRC have been developed, such as genetic deficient models (e.g., Muc2−/−, Msh2−/−, IL10−/−, p53−/−, etc.), chemical carcinogen-induced models (e.g., AOM/DSS, 1,2-DMH), and inoculation models [48], to evaluate features of CRC in humans, and have been widely used to determine the underlying mechanisms of carcinogenesis and to evaluate the effective prevention and therapy, but none of them is a perfect model. This evidence concerns the gene TP53 and colorectal carcinoma.