Upon release, eIF4E binds the scaffolding protein eIF4G1 and the RNA helicase, eIF4A, to form the eIF4F protein translation initiation complex that binds to the 5’ cap of certain mRNAs and facilitates cap-dependent translation.4–6 Phosphorylation of 4E-BP1 correlates with high risk in B-ALL and chronic lymphocytic leukaemia,3,7 while mTOR inactivation impairs B-ALL survival.8,9. The gene discussed is EIF4E; the disease is precursor B-cell acute lymphoblastic leukemia.