ACVR2B and Splenomegaly: Studies of a modified activin type IIb receptor-Fc fusion protein that inhibits Smad2/3 signaling decreased iron overload, splenomegaly, and bone pathology in murine β thalassemia, and in preliminary studies of sickle transgenic mice (ASH 2014, abstract 113, Modified ActRIIB-mFc Fusion Protein (murine ortholog of Luspatercept) Mitigates Sickling and Red Cell Pathology in a Murine Model of Sickle Cell Disease), reduced some markers of hemolysis, irreversibly sickled cells, membrane exposure of phosphatidylserine and splenomegaly [20].