AKT1 and neoplasm: Given that CD133 phosphorylation is crucial to mediate PI3K/Akt signaling, its dephosphorylation is an event that could restrict its function; Shimozato et al. (2015) identified that PTPRK (receptor-type protein tyrosine phosphatase K) interacts with CD133 and negatively regulate Akt activation [62], whereas its knockdown enhances tumor growth and survival due to CD133 ectopic expression in CRC under nutritional and cytotoxic stress [63, 64].