FLT3 and acute myeloid leukemia: Taken together, these results suggested that the phosphorylation of STAT5, driven directly or indirectly by BCR-ABL1 (in CML) and FLT3-ITD (in AML), could transcriptionally up-regulate the expression of miR-21 and, in turn, contribute to the subsequent regulation of PDCD4, among other miR-21 targets.