DNMT3A and acute erythroid leukemia: Interestingly, the gene expression signatures of the leukemic cells suggested functional interference with GATA1-regulated erythroid differentiation.114 Both of these studies demonstrated functional cooperation of Bcor alterations with Trp53 and/or Dnmt3A in mice; however, BCOR mutations seemed to be very rare events in human AEL.14–21 Interestingly, murine Bcor/Trp53-mutated AEL cells were sensitive to the PARP inhibitor talazoparib and the demethylating agent decitabine, and combined Trp53/Bcor/Dnmt3a mutation conferred sensitivity of AEL cells to CDK7/9 inhibitors.103