DNMT3A and myelofibrosis: Further studies could prove a pivotal role of TNFα and interferon α (IFNα) secretion and the activation of pro-inflammatory signaling pathways for driving myelofibrosis in EZH2/JAK2V617F-mutant myeloid progenitor cells or increased TNFα signaling in DNMT3A/JAK2V617F-mutant myeloid stem and progenitor cells [49,50].