AML disrupts normal DC development, characterised by an accumulation of arrested DC precursors (Lin−HLA‐DR+CD11c+CD123+) and a deficiency of terminal DC subsets (BDCA‐1+/BDCA‐3+mDCs; BDCA‐2+pDCs) in FLT3‐ITD+ patients at diagnosis. This evidence concerns the gene THBD and acute myeloid leukemia.