Recent studies identified the ERK kinase and the cyclin-dependent kinase CDK1 as important players of FLT3-ITD AML differentiation arrest through phosphorylation of the C/EBPα transcription factor on its serine 21 [14–16], suggesting that CDK or ERK inhibitors could restore the differentiation program of these cells. This evidence concerns the gene CEBPA and acute myeloid leukemia.