AKT1 and lymphoma: These types of inhibitors compete with ATP in the catalytic site of mTOR, inhibiting the function of both mTORC1 and mTORC2 and blocking the feedback Akt and eIF4E activation.[12] We recently demonstrated that the cytotoxic and antiproliferative effects of dual mTOR inhibition were more effective than rapamycin at inhibiting malignant cell proliferation and inducing apoptosis.[13] The present study was designed to comprehensively evaluate the role of the eIF4F complex in aggressive lymphoma cell growth and learn if dual mTOR inhibitor could inhibit eIF4F complex mediated mRNA translation.