AML (and cancer cells in general) rely on cap-dependent translation of oncogene mRNA transcripts,34,35 which exhibit mRNA secondary structures (such as G-quadruplexes) that require unwinding by the eIF4F complex helicase eIF4A.36 AML blasts overexpressing eIF4E become addicted to it, and treatment with ribavirin—a drug mimicking mRNA methylguanosine cap (m7G) and blocking eIF4E—inhibits tumor growth.62,63 In line with this, we found that xenografted hAML reflects a preference toward the cap-dependent translation of pro-tumorigenic transcripts (high GC content and short 5′ UTRs). This evidence concerns the gene EIF4A1 and acute myeloid leukemia.