JAK2 and myelofibrosis: The discovery in 2005 of the activating V617F mutation in Janus kinase 2 (JAK2) in the majority of patients with classic Philadelphia chromosome negative myeloproliferative neoplasms (MPNs)1, 2, 3, 4 led to the development of small-molecule inhibitors of the JAK family of tyrosine kinases, culminating in the regulatory approval of ruxolitinib in 2011 for the treatment of myelofibrosis (MF).5