However, inactivation and mutations in TP53 have also been associated with post-MPN acute myeloid leukemia (AML) transformation (in 25%-50% of cases) [10–13], suggesting that inactivation of the TP53 tumor suppressor could be a cooperating contributing event in combination with signaling due to JAK2 gain-of-function mutation during the transformation process. This evidence concerns the gene JAK2 and myeloproliferative disorder.