We hypothesised that BMP inhibition might recapitulate the anabolic effects of anti-sclerostin antibodies in myeloma bone disease in vivo, since: (a) osteocyte-secreted sclerostin is a major mediator of the osteogenesis block in myeloma;45 (b) anti-sclerostin antibodies ‘activate’ quiescent BLCs to become thicker, active and produce bone matrix in vivo5 and (c) both Acvr1 and Bmpr1a knockout in vivo decreased Sost and Dkk1 transcription32,39. This evidence concerns the gene BMPR1A and plasma cell myeloma.