It is proposed that interferon may be an active agent in the treatment of patients with idiopathic myelofibrosis. In this disorder the megakaryocyte cell lineage plays a major role in the deposition of bone marrow collagen by the release of growth promoting factors, including platelet-derived growth factor, which are mitogenic for fibroblast proliferation. Interferon reduces collagen deposition in the bone marrow by suppressing the activity of the proto-oncogene, which is involved in the production of growth factors from abnormal megakaryocytes and platelets. A direct myeloid cytoreductive effect of interferon upon the megakaryocyte proliferation contributes to reducing growth factor activity in the bone marrow. Finally, interferon induces monocytoid differentiation, thereby increasing bone marrow collagenase-activity. Thus, interferon has several actions, which in concert might reduce bone marrow collagen in myelofibrosis.