The Thrombopoietin Receptor (TpoR) is a central player in Myeloproliferative Neoplasms (MPNs). Mutations in JAK2, calreticulin or in TpoR itself drive constitutive activation of TpoR and uncontrolled proliferation and differentiation of hematopoietic stem cells and progenitors. The JAK2 V617F mutation is responsible for the majority of MPNs and all driver mutants induce pathologic TpoR activation. Existing therapeutic strategies have focused on JAK2 kinase inhibitors that are unable …