DISCUSSION: Several conditions can lead to EMH including primary / secondary myelofibrosis, thalassemia, and sickle cell anemia. The pathogenesis of EMH is poorly understood. It may represent differentiation of embryonic hematopoietic stem cells or the abnormal release of marrow precursors into the circulation. Radiology characteristics are variable and are at best suggestive of pulmonary EMH. Chest CT features are highly non-specific and include diffuse bilateral ground glass opacities, interstitial septal thickening, masses, or nodules. The colloid labeled with Technetium is taken up by macrophages and it also highlights erythopoietic activity. However, as seen in this case, false negatives do occur particularly if there is little medullary stroma present or if there is low cell activity. There are several pathophysiologic mechanisms implicated in the development of PH in patients with myeloproliferative neoplasms, including chronic thromboembolic PH (CTEPH) and pulmonary myeloid infiltration. Aberrant JAK-STAT signaling pathway may also contribute to the pathogenesis of PH in myelofibrosis by cultivating cultivating a hyper-proliferative apoptosis resistant state for pulmonary vascular endothelial cells (PAECs) and by depleting its nitric oxide (NO) stores.