JAK2 plays a critical role in the survival of MPN clone. Excision of Jak2 following disease establishment led to reduction in (A) WBC, (B) platelets, (C) spleen sizes, and (D) GFP-positive cells in BM (P < .005). Loss of JAK2 results in significant improvement in disease features including (E) restoration of splenic architecture, (F) decrease in myeloid infiltration in liver, and (G) reduction in BM fibrosis. (H) There was also a reduction in CD11b⁺Gr1⁺ cells and MEP population in MPLW515L-transduced mice lacking Jak2. (Data are represented at mean ± SEM; Jak2^+/+, n = 5; Jak2^−/−, n = 6).