We further confirmed that STING could interact with SEL1L and HRD1 in STING-proficient 5TGM1 multiple myeloma cells (Figs. 4d and S8C)28 and that the degradation of the BCR could be blocked by kifunensine (an ERAD inhibitor) or MG132 (a proteasome inhibitor) (Fig. 4e, f). This evidence concerns the gene SEL1L and plasma cell myeloma.