The most common oncogenic drivers of CRC include loss of function (LoF) (by mutation or deletion) of the tumor suppressors APC and TP53, and activating mutations in KRAS or BRAF. Less common but occurring in ~8–9% of CRC are non-synonymous mutations in the tumor suppressor PTEN5, a lipid phosphatase that is a negative regulator of PI3K/AKT/mTOR signaling. This evidence concerns the gene KRAS and colorectal carcinoma.