This phenomenon can be explained by three possible scenarios: firstly, the evolution of a synchronous leukemic clone, independent from the actual MPN; secondly, the loss of JAK2 mutation in the leukemic clone, as it might provide a differentiation signal hindering transformation; or thirdly, the presence of a common, clinically inapparent, pre-JAK2 clone, e.g., with common clonal hematopoiesis of indeterminate potential (CHIP)-type mutations to give rise to both MPN and AML [32,33]. This evidence concerns the gene JAK2 and myeloproliferative disorder.