Furthermore, OCT4 has been demonstrated as a direct substrate of AKT in mESCs14, hESCs15, mouse embryonal carcinoma cells (ECCs)16, human ECCs17, 18, and human CSCs18, 19, and AKT-phosphorylated OCT4 can regulate the transcription of AKT1 in a positive feedback manner to over-activate the AKT-OCT4 regulatory circuit and thereby promoting the anti-apoptosis pathways and survival of hECCs17. This evidence concerns the gene AKT1 and carcinoma.