FLT3-ITD: this is a common AML mutation associated with chemoresistance and reduced AML-free survival. It shows constitutive signaling and causes activation of CDC25. Normal myeloid differentiation requires activation of the transcription factor C/EBPα; constitutively activated FLT3-ITD causes an inhibitory phosphorylation and thereby a block of differentiation mediated either by ERK1/2 or by CDK1 (see description of the G2 phase, Table 4) [127,128,129]. This evidence concerns the gene FLT3 and acute myeloid leukemia.