Rampal et al. found that TP53 mutations were more common in JAK2 V617F-mutated specimens in the blast phase than in chronic phase MPN; the TP53 allele burden was >50% at the time of leukemic transformation (vs. 7% in the chronic phase), and TP53 nullizygosity potently cooperated with JAK2 V617F to induce leukemic transformation in paired patient specimens [41]. The gene discussed is JAK2; the disease is myeloproliferative disorder.