MPNs are defined by an uncontrolled proliferation of terminally differentiated cells of the myeloid lineage, the presence of driver mutations in the Janus kinase 2 (JAK2), calreticulin (CALR) or thrombopoietin receptor (MPL or TPOR) genes, an absence of the BCR::ABL1 disease marker, and an elevated risk of thrombotic as well as bleeding events, in addition to a propensity for the progression of PV or ET to secondary MF (SMF) or of all classical MPNs to evolve into acute myeloid leukemia (AML) [1,2,3,4]. Here, JAK2 is linked to acute myeloid leukemia.