In previous studies using the Ba/F3 pro-B cell line, and COS-7 cells expressing the WT and truncated G-CSFR forms, we demonstrated that ligand internalization and down-modulation of G-CSFR expression were impaired in cell lines expressing the Δ716 G-CSFR, which is the most common mutant G-CSFR form identified in patients with AML and antecedent SCN [17]. This evidence concerns the gene CSF3R and acute myeloid leukemia.