It is likely that FLT3-ITD contributes to increased proliferation of DC precursors as was shown in a mouse model by Lau et al. [40], but maturation of cDC subsets is altered in active AML due to cytogenetic aberrations or an abnormal cytokine milieu, which may induce an MDSC-like phenotype in DC precursors and prevent their final maturation. The gene discussed is FLT3; the disease is acute myeloid leukemia.