In osteoporotic patients, anti‐sclerostin therapy (Romosozumab) was associated with a lower risk of fracture26 but was also associated with potential adverse cardiac events.27 In addition, the positive effects of anti‐sclerostin therapy upon bone formation were only sustained for a short period.26 Furthermore, a combination of Dkk‐1 and sclerostin inhibition using a bi‐specific antibody approach demonstrated great promise at increasing bone formation and bone strength in naïve rodents and therefore would be a desirable method to test in preclinical models of myeloma.28 This evidence concerns the gene SOST and plasma cell myeloma.