Previous research has demonstrated that FLT3’s molecular chaperone, heat-shock protein 90, is substantially expressed in FLT3-ITD (+) AML and other malignancies.[74,75] In vitro and in vivo studies on FLT3-ITD (+) AML revealed a strong antileukemic effect when HHT and the heat-shock protein 90 inhibitor IPI504 were combined.[7] Mechanistically, apoptosis and cell arrest at G1 were brought on by the synergistic inhibition of FLT3 protein and its downstream AKT, STAT5, ERK, and 4E-BP1 by HHT and IPI504. This evidence concerns the gene EIF4EBP1 and acute myeloid leukemia.