Finally, very recent data suggests that the myeloproliferative neoplasm induced by truncation mutations of calreticulin also require c-Mpl to induce disease; in this case, elimination of the endoplasmic reticulum tether allows calreticulin to bind to c-Mpl and travel to the cell membrane where the thrombopoietin receptor dimerizes and drives Jak2 activation [29]. This evidence concerns the gene CALR and myeloproliferative neoplasm.