To better define the role of TP53 in the JAK2V617F phenotype and the impact of TP53 inactivation in MPN evolution and the response to treatment to reduce the clonal size, we studied mice with Trp53 inactivation and JAK2V617F endogenous mutation presenting a full phenotype of MPN (i.e., thrombocytosis, polycythemia, and leukocytosis). The gene discussed is TP53; the disease is thrombocytosis disease.