The discovery of Janus kinase 2 (JAK2) as a vital mediator of IE and splenomegaly in β-thalassemia indicated that the application of small organic molecules to inhibit JAK2 could reduce IE and splenomegaly.[57,58] Treatment of an erythropoietic disorder with an agent limiting erythropoiesis may seem counterintuitive. The gene discussed is JAK2; the disease is Splenomegaly.