Charlet et al. (2022) knocked down CSF2RB in AML cell lines with FLT3-ITD mutation and also transfected CSF2RB-deficient mice with FLT3-ITD mutation. The result was decreased STAT5 phosphorylation, reduced cell proliferation, and increased FLT3 inhibition sensitivity. In addition, the onset of the disease was delayed in the transfected mice, and there was an increase in the survival rate. They concluded that CSF2RB can be used to treat AML with FLT3-ITD mutation by discovering therapeutic peptides to target and interfere with FLT3-ITD-dependent CSF2RB activation (Charlet et al., 2022). This evidence concerns the gene CSF2RB and acute myeloid leukemia.