In CRC, the amplification of receptor tyrosine kinase12 as well as the frequent mutations in upstream regulators of AKT such as KRAS (mutated in 30%–40% of CRC cases) and PIK3CA (mutated in 10%–15% of CRC cases) lead to the constitutive activation of AKT signaling13,14. This evidence concerns the gene AKT1 and colorectal carcinoma.