In this regard, two preclinical studies with the heat shock protein-90 (HSP90) inhibitors PU-H71 40 and AUY-922 41 showed marked degradation of JAK2 in MPN cellular models, including JAK2 inhibitor-persistent cells 42, consistent with JAK2 being a client protein of the HSP90 chaperone complex; HSP90 inhibition normalized blood cell count, reduced allelic burden and improved survival in mice 40. The gene discussed is JAK2; the disease is myeloproliferative disorder.