While resistance has primarily been associated with antigen loss by acquired deletions or mutations [2–4], epigenetic target inactivation [5, 6], T-cell exhaustion [7] and an immunosuppressive microenvironment at baseline [8], translational data from the MajesTEC-1 trial indicates that elevated plasma levels of soluble BCMA (sBCMA) in MM patients with high tumour burden may impair antibody binding and can result in a dysfunctional effector:target (E:T) ratio [9]. The gene discussed is TNFRSF17; the disease is Miyoshi myopathy.