The advent of tyrosine kinase inhibitors targeting the leukaemogenic tyrosine kinases offered great hope; however, despite their ability to induce durable cytogenetic and molecular responses, they are rarely curative in chronic myeloid leukaemia (CML) and never in other MPNs.9 JAK2 inhibitors offer significant benefits in terms of symptom reduction10, 11 but few patients display reduced allele burden.12, 13 Thus, the development of knowledge of molecular pathogenesis mechanisms for the MPNs offers opportunities to inform potential new treatment strategies. Here, JAK2 is linked to chronic myelogenous leukemia, BCR-ABL1 positive.