Among the first candidates were other myeloproliferative diseases where the discovery of the activating JAK2 V617F mutation was considered ‘analogous’ to the Bcr-Abl translocation in CML.19 Notably, a number of other genetic variants/mutations have been linked to cases of de novo acute myeloid leukaemia (AML) and myeloproliferative neoplasm-blast phase, which all result in hyperactivated JAK-STAT signalling.28 This evidence concerns the gene SOAT1 and acute myeloid leukemia.