In this case, new therapies for MPN may be rewarded by a focus on agents that specifically target the mutant forms of JAK2 or CALR, or that specifically disrupt their productive interaction with Mpl, rather than on targeting pathways common to both normal and diseased Mpl signalling where there may be a significant challenge of disrupting diseased cells while sparing normal hematopoiesis. This evidence concerns the gene JAK2 and myeloproliferative neoplasm.