If these results were validated, it is of interest to note that the JAK2/MPL-independent alterations triggered by mutant calreticulin in our worm model do not seem to be responsible for the initiation of the disease, since the introduction of patient-like calreticulin mutations in in vivo models that lack or have a decreased expression of MPL are unable to induce an MPN [39,40]. This evidence concerns the gene JAK2 and myeloproliferative disorder.