While in AML and MDS, PLK2 is similarly methylated, although the PLK2 methylation status has no significant effect on clinical indicators and long-term prognosis (90); Additionally, in myeloproliferative neoplasm (MPN) like MDS, the disordered co-expression and disrupted signal transduction of PLK2 with myeloid tumor suppressor Egr1 and JunB may be a pathogenesis (91). This evidence concerns the gene JUNB and myeloproliferative disorder.