Based on a recent report implicating CEBPA as a key regulator of FLT3 expression in AML [43] as well as previous studies suggesting that promotion of granulocytic differentiation by CEBPA is inhibited in FLT3-ITD AML via ERK1/2- or CDK1-mediated phosphorylation of serine-21 [22, 44], we examined whether CEBPA phosphorylation is modulated by TOPK activity. Here, PBK is linked to acute myeloid leukemia.