An alternative pathway for activation of CDK1 is the constitutive activation by FLT3-ITD; this signaling can activate both ERK1/2 and CDK1 and these kinases can then phosphorylate the transcription factor C/EBPα; this phosphorylation will inhibit its transcriptional activity and thereby contribute to the differentiation block in these AML cells [127,128,129]. This evidence concerns the gene CEBPA and acute myeloid leukemia.