AML cells carrying the poor prognosis internal tandem duplication (ITD) activating mutation in the FLT3 tyrosine kinase are specifically dependent on glutamine metabolism, both as a fuel for TCA cycle and precursor of gluthatione necessary for ROS scavenging, and glutaminolysis inhibition rescues resistance to FLT3 inhibitors (27). This evidence concerns the gene FLT3 and acute myeloid leukemia.