Since we have observed that 3-AWA regulated eIF4E through modulation of Ras-Mnk and PI3K-AKT-mTOR pathways, here, this dual modulation by 3-AWA exhibits an excellent advantage of preventing the increase in eIF4E phosphorylation during mTOR inhibition that might otherwise, counteract mTOR inhibitor’s growth inhibitory effect in cancer cells. The gene discussed is MTOR; the disease is cancer.