Previously, IL‐6 has been shown to be upregulated in myeloma patient sera59 and by BMSC, particularly when in contact with myeloma cells,57 and IL‐6 is thought to increase the proliferation/differentiation of osteoclasts.60 TGFβ is also known to upregulate the production of IL‐6 by BMSC, the effect of which can be blocked using a TGFβ signaling antagonist (SD‐208, a small molecule inhibitor).37 Therefore, TGFβ in myeloma is also likely to contribute to bone disease by upregulation of IL‐6 in the BMME. This evidence concerns the gene TGFB1 and plasma cell myeloma.