JAK2 and myelofibrosis: Myelofibrosis arises predominantly from mutations in hematopoietic stem and progenitor cells (HSPCs) that activate Janus kinase 2 (JAK2), and resistance to standard-of-care JAK2 inhibitors (Ruxolitinib, Fedratinib) has been shown as a consequence of concomitant activation of compensatory PI3K and MAPK survival signaling25–27.