Other genetic and pathway alterations involved in erythroid differentiation likely play a cooperative role in the disease’s development.[13] For instance, EZH2 mutations have been linked to aberrant erythropoiesis in patients with primary myelofibrosis (PMF), manifesting as impaired erythroid progenitor maturation and cell cycle arrest.[14] In our case, the comorbidity of EZH2 mutations with the TP53 frameshift mutation could have contributed to a more aggressive PEL phenotype with compromised erythroid differentiation. This evidence concerns the gene TP53 and primary myelofibrosis.