In CML and other malignancies, sustained activation of mTOR kinases affects the function of two important regulators of translation, S6 kinase (S6K1) and the initiation factor-binding protein 4E-BP1, which become hyperphosphorylated in an mTOR-dependent manner; as a result, 4E-BP1 is inhibited while S6K1 and cap-dependent translation are activated (figure 1a) [21,22]. The gene discussed is MTOR; the disease is chronic myelogenous leukemia, BCR-ABL1 positive.