We test for the JAK2 gene without bone aspiration, using only peripheral blood. The JAK2 gene is located on chromosome 9p24 and encodes a tyrosine kinase containing a self-repressing structural domain that functions in the JAK-STAT signaling pathway.JAK2 mutations are seen almost exclusively in hematologic tumors, and although some patients with JAK2 V617F mutations develop with symptoms of deep vein thrombosis such as Boo-ga syndrome, these patients are still essentially hematologic disorders. JAK2 V617F mutations are seen in 95% of true erythrocytosis (PV), about half of thrombocytosis (ET) and primary myelofibrosis (PMF); JAK2 exon12 mutations are mainly seen in JAK2 V617F-negative PV; JAK2 gene in ALL is mainly a mutation of Exon16, mostly seen in BCR-ABL1-like ALL. JAK2 can also be involved in acute lymphoblastic leukemias such as BCR-ABL1-like ALL by forming fusion genes due to gene translocations. Related diseases and other related tests 1. Related diseases: MPN; PV; ET; PMF; B-ALL; T-ALL; BCR-ABL1-like ALL. 2. Somatic mutations JAK2-V617F mutation: seen in 95% of true erythroblastosis (PV), about half of thrombocytosis (ET) and primary myelofibrosis (PMF), about 2% of of MDS, approximately 26% of MDS/MPD-U, approximately 66% of RARS-T, and approximately 7% of CMML/aCML patients. JAK2 V617F mutation, essentially MPN, was detected in about 50% of patients with hepatic portal vein thrombosis or Buga syndrome as clinical manifestations. JAK2-exon12 mutation: mainly seen in JAK2 V617F-negative PV. Mutated JAK2 protein loses its self-inhibitory activity, exhibits hypersensitivity to EPO, and also evades the negative SOCS3 inhibitor Patients with JAK2 mutations are effectively treated with the kinase inhibitor ruxolitinib (Jakafi).