We show that this persistent STAT3 phosphorylation and activation in the injured muscle is an important driver of NHO as administration of ruxolitinib, a small synthetic inhibitor of JAK1/2 tyrosine kinases used to treat myelofibrosis and polycythemia vera caused by activating mutations of JAK2 (27, 28), significantly reduced STAT3 phosphorylation in the injured muscles of mice. Here, STAT3 is linked to acquired polycythemia vera.