Abstract
Enthusiasm about interferons for the treatment of myeloproliferative neoplasms has recently arisen. How does a nontargeted therapy selectively target the malignant clone? Many foundational questions about interferon treatment are unanswered, including who, when, and for how long do we treat. Using an individual case, this review touches on gaps in risk assessment in polycythemia vera (PV) and essential thrombocythemia (ET) and the history of treatment with interferons. How is it that this proinflammatory cytokine effectively treats ET and PV, themselves proinflammatory states? We summarize existing mechanistic and clinical data, the molecular context as a modifier for treatment response, the establishment of treatment goals, and the challenges that lie ahead.