In two myeloma mouse models, the administration of an Activin A chimeric inhibitor (RAP-011) derived from the fusion of the extracellular domain of activin receptor IIA and the constant domain of the murine IgG2a [126] or a soluble Activin A receptor type IIA fusion protein (ActRIIA.muFc) blocks the development of osteolytic bone lesions by both inhibiting OC development and stimulating osteoblastogenesis [80, 127]. The gene discussed is ACVR2A; the disease is plasma cell myeloma.