They dysregulate fewer genes than men [66] and have fewer cytogenetic abnormalities [67,68], acquire PV or ET earlier than men [69], have a discernably different thrombotic diathesis than men [70], a lower risk of transformation to JAK2 V617F mutation-positive myelofibrosis [71], a lower JAK2 V617F mutation allele burden than men, and a longer survival than men [72]. Here, JAK2 is linked to myelofibrosis.