TP53 and acute myeloid leukemia: A subset of MPN patients progress to AML that is associated with recurrent somatic alterations affecting epigenetic regulators, splicing-related factors and/or the TP53 tumor suppressor.106 To demonstrate potential cooperation, researchers retrovirally overexpressed JAK2V617F in either wildtype or Trp53−/− BM-derived HSPCs and transplanted them into irradiated wildtype recipients.23,100 Mice developed a serially transplantable leukemic phenotype with hepatosplenomegaly with infiltration of CD71+/Ter119− erythroid progenitor cells.