JAK2 is a non-receptor tyrosine kinase that mediates signal transduction from multiple cytokine receptors including those for erythropoietin, growth hormone, prolactin, and interferons 12. Upon ligand binding, JAK2 phosphorylates specific tyrosine residues on receptor cytoplasmic tails, creating docking sites for STAT proteins, which JAK2 then phosphorylates 13. Activated STATs translocate to the nucleus to drive gene transcription regulating cell growth, differentiation, and immune responses 1. JAK2 also functions in chr9 regulation by phosphorylating histone H3 at tyrosine 41, promoting CBX5 exclusion and chr9 remodeling 4. Acquired JAK2 mutations, particularly the V617F mutation in exon 14 and various exon 12 mutations, cause myeloproliferative neoplasms (MPNs) including polycythemia vera, essential thrombocytosis, and primary myelofibrosis 56. These mutations constitutively activate JAK2 kinase activity, driving excessive erythropoiesis and thrombocytosis 5. JAK2 mutations are also associated with Budd-Chiari syndrome through mechanisms including endothelial damage and increased blood cell adhesion 7. JAK2 has emerged as an important therapeutic target in MPN management 89.