Our finding of upregulated AKT activation in CRC cells by the PP2A-B56γ3 holoenzyme was similar to the finding that cancer cells treated with mTOR inhibitors, such as rapamycin and Torin, exhibited hyperactivation of PI3K/AKT signaling by attenuating mTOR/p70S6K-mediated negative feedback loops [38]. The gene discussed is AKT1; the disease is colorectal carcinoma.