Although others have shown that disrupting translation with inhibitors of upstream signal transduction (imatinib for Bcr-Abl, PP242/INK148 for mTOR (mammalian target of rapamycin)) reduces the transformation properties of CML cell lines and patient cells, we propose that hippuristanol inhibition of translation directly targets a special eIF4A dependence of the IRES-containing class of mRNAs [16–18]. This evidence concerns the gene MTOR and chronic myelogenous leukemia, BCR-ABL1 positive.