The observation that HHT, a widely marked anti-cancer agent (28–30), specifically antagonizes p-eIF4E function and inhibits growth of AML cells expressing high levels of p-eIF4E by targeting the phosphorylated serine 209 residue of p-eIF4E, but not for eIF4E, for SUMO2/3-mediated degradation is somewhat unexpected and of particular interest. This evidence concerns the gene SUMO2 and acute myeloid leukemia.