In the nucleus, a hyperactive JAK2 induces phosphorylation of the histone H3 at tyrosine residue 41 (H3Y41), releasing the transcriptional repressor heterochromatin protein 1alfa (HP1a) from chromatin and resulting in an activation of transcription of genes repressed by HP1a, as the oncogene LMO2. LMO2 might play a role in the pathogenicity of MPN. Here, JAK2 is linked to myeloproliferative disorder.