To the best of our knowledge, there are no mutational data, such as high-copy gene amplification, gene fusions and translocations, or recurrent localized missense mutations that establish clear-cut gain-of-function defects for SOX9 in CRCs, which are the types of genetic data needed to support a role for SOX9 as an oncogene in CRC biology, akin to the genetic evidence that exists for known oncogenes, such as MYC, KRAS, and BRAF. This evidence concerns the gene KRAS and colorectal carcinoma.