Accordingly, MplIC36/IC36 mice were indistinguishable from Mpl−/− mice: steady-state megakaryopoiesis was compromised, recovery of platelet numbers following 5-FU was attenuated, HSC function was defective, and MplIC36/IC36 mice failed to develop features of MPN driven by mutations in Jak2 or Calr. Previous analysis of knockin mice lacking the C-terminal 60 cytoplasmic Mpl residues (Δ60 mice), retaining both Box1 and Box2, reported normal receptor expression [6]. This evidence concerns the gene JAK2 and myeloproliferative disorder.