[10], [11]. The molecular mechanisms of myeloproliferative neoplasm (MPN) converting into AML were examined in 330 cases [12]. Among the 22 patients with transferred to AML, 10 (45.5%) cases had evidence of a p53-related defect mediated by gains (amplification) of chromosome 1q (which contains the potent p53 inhibitor MDM4) or TP53 gene mutations. These reports suggest that overexpression MDM4 may be involved in the leukemogenic mechanisms of CK-AML patients without TP53 alterations. Here, TP53 is linked to acute myeloid leukemia.