However, in other hematological malignancies such as FLT3-mutated AML or JAK2-associated myeloproliferative neoplasms, extremely powerful and specific kinase inhibitors (quizartinib or ruxolitinib) have not had a similar impact, probably because in neither case the targeted mutation is in the founding leukaemia clone. This evidence concerns the gene JAK2 and myeloproliferative disorder.