This mechanistic hypothesis is also compatible with the already widely known evidence that patients with the CALR mutation generally have a better prognosis than patients with JAK2-mutation [47], and adds the evidence that the assessment of response to oxidative damage, showed here using an easy plasma assay, could provide an additional variable to better define the prognosis of patients with myelofibrosis. This evidence concerns the gene JAK2 and myelofibrosis.