Since preliminary studies have highlighted the suitability of eIF4A as a therapeutic target in different hematological malignancies both in vitro and in vivo [42, 43], we sought to evaluate the effect of the eIF4A inhibitor (eIF4Ai) CR-1-31-B on AML survival, mRNA translation and mitochondrial function, both as single agent and in combination with araC [44]. The gene discussed is EIF4A1; the disease is acute myeloid leukemia.