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. The gene discussed is IL6; the disease is plasma cell myeloma.